Approach To Headache

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Approach to Headache
Updated: October 9th 2022
Approach to Headache
Authors
 Nick Ashenburg, MD
 Evadne Marcolini, MD
 Jason Hine, MD
Associate Editor
 Megan Fix, MD
Editors in Chief
 Amal Mattu, MD
 Stuart Swadron, MD
Rapid Access
Approach to the Critical Patient
The General Approach

 Consider the critical diagnoses
 Assess ABC’s
 Focused history and physical exam.
o Assess vital signs - headache with abnormal vital signs (particularly
fever or elevated blood pressure) can indicate a life-threatening
diagnosis.
 Fever may indicate an infectious etiology such as meningitis,
brain abscess, or encephalitis. Additionally, a significant
percentage of patients with giant cell arteritis will present with
fever.
 Significantly elevated blood pressures and headache may
indicate intracranial hemorrhage, hypertensive encephalopathy,
posterior reversible encephalopathy syndrome (PRES), or pre-
eclampsia in a pregnant patient.
 A patient with irregular respirations, bradycardia, and
hypertension may be suffering from increased intracranial
pressure (this triad is referred to as Cushing reflex). This may
indicate intracranial hemorrhage, idiopathic intracranial
hypertension, cerebral venous thrombosis, or stroke.
o Take a focused history - At a minimum, patients should be asked
about the onset, location, and severity of their headache, as well as
associated symptoms, allergies, and medications.
 Keep in mind the SNOOP2 mnemonic as it prompts the
physician with key considerations.
 >90% of patients with subarachnoid hemorrhage
(SAH) will report a sudden, severe headache, and
30% of the time this headache will lateralize to the
side of the head.
 Of those that report a thunderclap headache
(maximizing within 1 minute from onset), 11-25% will
have a SAH.
 Fever, neck pain, or altered mental status is present
in 99-100% of patients with meningitis; therefore, the
absence of all three of these symptoms or exam findings
is reassuring.
 Age is a risk factor for pathology:
 The rate increases to 11% among patients
older than 75.
 Patients older than 50 presenting with headache
have been shown to have a pathologic finding 6%
of the time compared to 1% of patients younger
than 50.
 Perform a physical exam, including a complete
neurologic exam, fundoscopic exam, and a head and
neck exam.
 A complete neurologic exam includes an assessment of
mental status and level of consciousness, cranial nerve testing
including pupillary responses and extraocular testing, strength
and sensation testing, cerebellar testing, gait testing, and
tendon reflexes.
 A focal neurologic deficit currently shows one of the
largest positive predictive values of intracranial
pathology.
 The U.S. Headache Consortium found that an
abnormality on the neurologic exam tripled (3x)
the likelihood of positive findings on
neuroimaging.
 Pay particular attention to vision testing and ocular
complaints. Extraocular muscle nerve palsies and
abnormal pupillary responses can be subtle and difficult
to detect, but can be key leads in making a diagnosis.
 Concerning exam findings
EM:RAP Link
 C3 - Headache
Key Concepts
 Headache accounts for nearly 3% of all ED visits.

 Headaches are classified as either primary or secondary, with secondary
headaches being a symptom of an underlying condition. Nearly 98% of
headaches in the ED are thought to be primary in nature or a benign
secondary headache.
 Prioritize the diagnosis/ruling out of dangerous causes of headaches that can
result in death or devastating injury to the brain, eyes, or limbs. Look for red
flags to identify patients with potentially dangerous causes of headache.
 Use a modified version of Dodick’s SNOOP mnemonic to elicit secondary
causes of headache.
 Alleviating pain does not mean that dangerous causes of headache have
been ruled out. That said, pain should be addressed promptly regardless of
the etiology of headache.
Critical Diagnoses
 Critical Diagnoses: The headaches you cannot miss

 Concerning exam findings
 DO NOT back away from the fundoscopic exam.
o This is a necessary exam to look for papilledema in anyone with a
headache and vision change. Though intimidating to some, the exam
is made significantly easier with dilated pupils (use 1 drop of 1%
tropicamide) and a panoptic ophthalmoscope if available.
 For a video demonstration of the exam and more information,
see Fundoscopic / Ophthalmoscopic Exam
o Ocular ultrasound is not perfect!
 While ocular ultrasound is great for identifying a number of
ocular emergencies, there is insufficient evidence for a
correlation between intracranial pressure and optic nerve
sheath diameter. If there is concern that the patient may have
increased intracranial pressure, follow through with plans for
brain imaging and lumbar puncture.
Diagnosis
 Laboratory testing and imaging can provide valuable information when

considering particular diagnoses.
 Providers need to be prudent when determining which patients warrant
further studies, as over-testing and over-utilization of resources can harm
patients both physically and financially and is burdensome to the health care
system.
o The SNOOP2 mnemonic, chart can help guide decision making
regarding appropriate lab testing and imaging.
o Established decision rules can help guide decision making after
obtaining a patient’s history and physical.
 The Ottawa Subarachnoid Hemorrhage Rule has been
found to be 100% sensitive but only 15.3% specific. If applied
correctly, it can effectively rule out SAH.
o The 2019 American College of Emergency Physicians (ACEP) policy
encourages the use of non-opioid analgesia over opioids in the
treatment of headache (Level A).
o The 2019 ACEP policy endorses the Ottawa Subarachnoid
Hemorrhage Rule, as well as the use of non-contrast CT within 6 h
of symptom onset, to rule out SAH (Level B).
o The 2019 policy provides a weaker recommendation (Level C) for the
use of CT angiography as an alternative to lumbar puncture in
scenarios where clinical concern for aneurysmal SAH persists despite
a negative non-contrast CT.
o The previous (2008) policy provides guidance for special scenarios
that may require further neuroimaging in the ED.
Disposition
 Disposition varies depending on facility and resources as well as severity of

disease.
 In general, patients with a critical diagnosis listed in Critical Diagnoses:
The headaches you cannot miss, warrant admission, most frequently an
ICU or step down unit.
 Rarely, patients with a diagnosis in Critical Diagnoses: The headaches
you cannot miss may be discharged home. This should only occur after
completion of a thorough workup and assessment, consultation with the
appropriate subspecialist, and a safe discharge plan with strict return
precautions in place.
 Most patients with primary headache can be discharged home after adequate
pain control.
Deep Dive
 Headaches are estimated to account for approximately 4 million ED visits
annually, which equates to almost 3% of all ED visits.
 The main goal in the ED is to provide safe and effective treatment to
alleviate headache while excluding the serious causes of headache.
 Approximately 2% of ED diagnoses for patients presenting with headache
are found to have a secondary cause of their pain.
Diving into the Can’t Miss Diagnoses
 A more thorough discussion of the data regarding epidemiology, history,

physical exam findings, diagnostics and management of critical diagnosis is
listed below. A discussion of benign but common causes of headache in the
ED is listed at the end.
Subarachnoid Hemorrhage
 Subarachnoid hemorrhage (SAH) refers to blood in the subarachnoid
space. This space is normally filled with cerebrospinal fluid (CSF) and
lies between the arachnoid and pia mater.
Background
Epidemiology
 SAH accounts for 5-10% of all strokes in the U.S. The victims tend to be
younger than average stroke patients; therefore, SAH results in more
productive years lost than other types of stroke.
 Though improving, the mortality rate remains high at 25-50%; notably, this
number does not include those that die before receiving medical attention.
Pathophysiology
 80% of non-traumatic or spontaneous SAH is caused by an aneurysm

rupture. Intracranial aneurysms are thought to be present in 1-2% of the
population. These aneurysms typically form at branch points of arteries and
wall segments, which are made weaker by hemodynamic stressors at the
branch point.
o Increased risk of the presence of aneurysms is associated with family
history, patients with connective tissue disorders, and polycystic
kidney disease.
o Increased risk of aneurysm rupture is associated with black race,
hispanic ethnic group, hypertension, current smoking, alcohol abuse,
sympathomimetic drugs, and aneurysm larger than 7 mm.
 Common causes of spontaneous SAH other than aneurysm include AV
malformations and vasculitis. However, up to 10% of nonaneurysmal SAH
involve no vascular abnormality.
Diagnostic considerations
Clinical presentation
 There is no single history or physical exam finding that significantly

increases or decreases the post-test probability.
 90% of patients with SAH will report a sudden, severe headache.
 Of those that report a thunderclap headache (maximum intensity within 1
min from onset), 11-25% will have a SAH.
 A sentinel bleed/headache or “warning leak” may occur in 10-40% in the
weeks leading up to the ED presentation.
 A systematic review found that a history of neck pain and neck stiffness on
exam increased the probability of SAH, while the absence of the “worst
headache of my life” or the onset of headache taking more than 1 h reduced
the probability of SAH (though the confidence interval crossed 1).
 Seizure or loss of consciousness at the time of onset are other well-
documented symptoms, though they occur in <50% of patients.
Decision Rule
 The Ottawa Subarachnoid Hemorrhage Rule has a sensitivity of 100%

and a specificity of 15% for the diagnosis of SAH.
Radiographic and Laboratory Evaluation
 Noncontrast CT is the initial study of choice and has been found in recent
literature to be nearly 100% sensitive if acquired within 6 h of the initial
onset of headache.
 ACEP and the AHA/ASA current guidelines recommend a lumbar puncture
(LP) following a normal noncontrast CT to rule out SAH irrespective of the
time of CT in relation to onset of headache. However, these guidelines have
not been updated since 2008, and the ACEP guidelines are currently under
review. An LP should be performed if there is concern and the patient is
outside the 6 hour window from symptom onset.
o Increasing research and deliberation have focused on determining if
CTA is a suitable substitute for an LP as an adjunct to non-contrast
CT to rule out SAH. However, there is currently insufficient evidence
to support such practice.
 An LP can be performed to search for blood or xanthochromia in the
cerebrospinal fluid CSF and thereby to make the diagnosis of SAH.
o A higher red blood cell (RBC) count in the last tube increases the
chances that there has been SAH. One study demonstrated that
<2,000 x 106/L RBC without xanthrochromia excluded SAH with
100% sensitivity.
o Xanthochromia is a yellow discoloration of CSF due to hemoglobin
breakdown products. If blood has been in CSF for >2 h,
xanthrochromia can be detected. LP performed before the 2 h mark
from the bleed may not demonstrate xanthochromia. Xanthochromia
alone does not confirm SAH. The presence of xanthochromia is
known to occur in cases of increased CSF protein, traumatic LP with
more than 100,000 RBCs, and systemic hyperbilirubinemia.
Therapeutic Considerations
 While in the ED:

o If SAH is diagnosed, consult a neurosurgeon and the Neuro ICU as
soon as possible.
o If the patient is taking anticoagulants, anticoagulation should be
reversed.
o Hypertension in the case of SAH is concerning because it increases
the risk of rebleeding; however, management is controversial. The
benefits of reducing blood pressure must be weighed against the risks
of decreasing cerebral perfusion pressure and therefore risking
infarction. The AHA/ASA guidelines suggest that a reduction of
systolic blood pressure by <160 mm Hg is reasonable. No specific
pharmacologic agent is recommended over others for blood pressure
control.
o After the patient has been stabilized, vascular imaging (CTA) should
be acquired to find the source of the bleed. However, do not delay
transfer to a higher level of care for further imaging, as it can be
performed as needed in the receiving hospital.
o Other considerations
 All patients with SAH should receive oral nimodipine 60 mg
by mouth every 4 h, as it has been shown to reduce the risk of
poor outcomes. Nimodipine decreases the risk of delayed
cerebral ischemia and improves neurologic outcome, though it
does not decrease the risk of vasospasm.
 Use of anticonvulsants remains under review, and the
AHA/ASA guidelines state that prophylactic anticonvulsants
may be considered in the immediate post-hemorrhagic period.
o Prognosis
 Rebleeding is the most feared complication and is most
common in the first 24 h.
 See chapter: Aneurysmal Subarachnoid Hemorrhage
Meningitis
 Meningitis can be caused by bacteria, vira, fungi, parasites, or non-

infectious agents. Bacterial meningitis is a significant concern due to its
high mortality rate.
Background
Epidemiology
 Central nervous system infections account for 0.5% of all headaches that
present to the ED.
 Rates of meningitis have decreased significantly with the advent of vaccines
(in particular, for Haemophilus influenzae type B and Neisseria
meningitidis). A recent review of ED visits for meningitis demonstrated that
it results in 66,000 visits per year, a rate of 62 per 100,000 visits.
o The estimated mortality rate of bacterial meningitis is thought to be
15%; it is estimated to kill approximately 135,000 people worldwide
each year.
Pathophysiology
 Bacterial Infections occur when organisms access the subarachnoid space,
most commonly through contiguous spread from a local infection or
bacteremia or a neurosurgical procedure.
 Fungal meningitis is much less common and nearly always affects
immunocompromised patients; however, it has been associated with steroid
injections used for treating pain.
 Viral meningitis, though usually less severe, is the most common form of
meningitis. Viral pathogens initially infect the respiratory or gastrointestinal
tract and ultimately seed the nervous system.
Meningitis vs Encephalitis
 Patients with meningitis often demonstrate normal brain function; however,

encephalitis is truly an infection of the brain
parenchyma. Encephalitis patients may present with abnormalities of brain
function.
o Please see viral encephalitis below for further review.
Diagnostic Considerations
Clinical Presentation
 Headache is present in 27-81% of patients suffering from bacterial

meningitis.
 A combination of headache, fever, and neck stiffness is taught as the
“classic triad” of meningitis but is present in only 44% of patients.
 The complete absence of fever, neck pain, or altered mental status greatly
decreases the suspicion of meningitis, as one of these three elements is
present in 99-100% of patients with meningitis.
 Other symptoms may include nausea, vomiting, rash, seizure, and potential
cranial nerve deficits.
 No single exam finding can accurately predict a diagnosis of meningitis.
o Physical exam signs of meningeal inflammation, namely nuchal
rigidity, Kernig’s sign, and Brudzinski’s sign, are not sufficiently
reliable to rule in or rule out meningitis. However, they are specific
(82-98%) and increase the clinical suspicion for meningitis when
present.
 Kernig’s: With the patient supine, flex the hip and the knee,
then extend the leg at the knee. The test is positive if extension
of the knee elicits resistance or pain in the lower back or
posterior thigh.
 Brudzinski’s: The test is positive if passive neck flexion in a
supine patient results in flexion of their hips and knees.
Jolt accentuation: The patient is asked to turn their head to the

left and right at a rate of 2-3 turns per second. The test is
positive if their headache is worsened with this maneuver.
 The provider’s clinical gestalt is crucial, as individual symptoms and
physical exam findings are not sufficiently sensitive.
 A patient suspected of having meningitis should undergo an LP, assuming

there is no contraindication (contraindications include possible raised ICP,
thrombocytopenia, bleeding disorders, anticoagulation therapy, or suspected
epidural abscess or overlying cellulitis).
 If bacterial meningitis suspicion is high, empiric antibiotic therapy should be
started immediately; do not delay for imaging or LP. The sensitivity of CSF
decreases with antibiotic administration, but the morbidity of this disease is
too high to justify the delay.
 Who should be imaged before LP?
o CT of the head should be obtained before LP in a patient who is at
risk for an intracranial mass or midline shift due to concern for brain
herniation as a result of LP.
 Absolute criteria for who should be subject to imaging have
not been determined, and various criteria exist. CT performed
before LP has been demonstrated to delay antibiotic use and
time to diagnosis. If there is concern for bacterial meningitis,
begin empiric antibiotics as soon as possible.
 Per the Infectious Disease Society of America (IDSA)
guidelines, pre-LP CT should be obtained in the following
patients:
 Immunocompromised
 CNS disease
 New onset seizure
 Altered consciousness
 Focal neurologic deficit
 Papilledema
 If CT is needed, the correct sequence should be:
 Antibiotics → CT → LP ASAP
o After LP, tests on CSF fluid should include:
 Cell count
 Gram stain
 Glucose
 Protein
 Herpes simplex virus (HSV) assays (PCR) should be
considered for all patients, but especially in the
immunocompromised, as should special tests for fungal
infections such as cryptococcal or mycobacterial infections.
 CSF profiles for normal fluid, bacterial, viral, and
fungal meningitis
 Other tests to consider in addition to LP:
o CBC, metabolic panel, coags, and blood cultures.
 Though not necessary, procalcitonin is a serum marker that is significantly
elevated in bacterial infections and has been shown to be helpful in
distinguishing bacterial from viral meningitis.
Bacterial Meningitis
 Treatment is aimed at the most likely pathogens. This will vary with the
population.
 Per a 2015 Cochrane review, corticosteroids should be considered as an
additional therapy in cases of suspected bacterial meningitis, and ideally
administered before or with antibiotics, as they have been shown to decrease
neurological sequelae and hearing loss.
 Initial antibiotics for suspected bacterial meningitis based on age.
 Disposition: Patients undergoing workup for bacterial meningitis should be
admitted to the hospital and placed in isolation.
Viral meningitis
 Treatment is primarily supportive, as there is no specific antiviral therapy

for most causes.
 HSV-1 and HSV-2 CNS infections are treated with acyclovir (10 mg/kg).
 Disposition: Patients with viral meningitis are often admitted to the hospital.
However, there should be discussion regarding which patients are safe for
discharge. Factors to consider include the general appearance of the patient,
the ability of the patient to tolerate oral hydration, concern for HSV
infection, pain control, social support, and circumstances.
Fungal meningitis
 Rarely found in patients other than the immunocompromised.

 If concern is high (immunocompromised host and history of fungal
meningitis), empiric therapy with amphotericin B should be initiated while
isolation of a specific fungus is performed.
o Steroid use is not recommended in fungal meningitis, as it is
associated with more adverse events and disability.
 Disposition: Patients with fungal meningitis should be admitted to the
hospital.
 See chapter: Central Nervous System Infection
Reversible Cerebral Vasoconstriction Syndrome

 Reversible cerebral vasoconstriction syndrome (RCVS) is associated with
acute onset and severe, recurrent headache typically occurring over 1-2
weeks. It can be found with or without neurological symptoms. RCVS is
thought to be due to a reversible vasoconstriction of cerebral arteries. These
patients are at increased risk of hemorrhagic or ischemic stroke, and the
preceding headache may be a “warning” sign requiring a modification of
risk factors.
Background
Epidemiology
 RCVS is the most frequent cause of “thunderclap headache” that is not

SAH, but the exact incidence is unknown.
 At least half of the cases are secondary to exposure of vasoactive substances
including illicit drugs, sympathomimetics or serotonergic drugs or in the
postpartum period.
 RCVS is more common in women than men. The average patient presents in
their 40s, though women tend to present older (50s) than men (30s).
Pathophysiology
 The exact pathophysiology of vasoconstriction is poorly understood but may

be due to either exogenous or endogenous factors such as drugs; tumors;
endocrine factors; trauma; as well as pregnancy-related, postpartum, or even
uncontrolled hypertension.
Diagnostic criteria
 The International Classification of Headache Disorders (ICHD-3) has

established criteria for headache attributed to RCVS.
 Thunderclap headache (reaches a maximal peak within seconds to minutes)

is reported in 95% of patients and is the only symptom in 75%. The
headache itself has been described as diffuse or localized, stabbing or
throbbing, and is associated with nausea, vomiting, photophobia, seizures,
and with or without neurologic signs such as visual changes, aphasia,
dysarthria, hemiplegia, or ataxia in various accounts.
o Most patients will experience 4-8 attacks over a 4-week period.
o 80% of patients will describe a headache trigger.
 Often triggered by exertional maneuvers, sexual activity,
valsalva, emotion, or bathing.
 MRA and CTA are appropriate imaging techniques to assess for RCVS.
Classically, angiographic findings reveal alternating areas of arterial
constriction and dilation referred to as “beading.” However, nearly half of
the patients will have a normal initial scan of their brain.
o 20% of cases will have normal CTA/MRA. A second imaging study
angiogram may be positive days later.
 Diagnosis is confirmed with evidence of reversibility of vasoconstriction
(“string of beads” appearance).
 Routine labs (CBC, metabolic panel, liver function tests) and CSF are
typically normal in RCVS.
Medical Management
 If RCVS is suspected based on history, exam, and/or imaging, consult a

neurologist.
o Termination of vasoactive substances should be considered, as should
any other potential aggravating or precipitating factors.
o Patients may be admitted based on imaging findings and the need for
blood pressure management.
o Though evidence is weak, calcium channel blockers are often
utilized, as they are thought to decrease the frequency and intensity of
headaches within 48 hours (30-60 mg every 4-8 h PO or 0.5-2
mg/kg/h).
 Glucocorticoids were previously encouraged, but more recent
evidence has raised concerns about worsening clinical course.
Prognosis
 Complications such as SAH, intracerebral hemorrhage (ICH), seizures, or

ischemic stroke may occur within 30 d of the initial ED visit in patients with
normal non-contrast CT in the ED.
o In one study, 17% of patients found to have hemorrhagic RCVS had
presented to the ED with isolated headache and normal imaging and
only afterward developed either SAH, ICH, or subdural hematoma.
Most of these events occur in the first 8 d after initial headache, but
these have been shown to occur as far out as 20 d.
 Adverse outcomes are primarily due to stroke.
Viral Encephalitis
 Encephalitis refers to inflammation of the brain parenchyma. These patients

present with abnormalities of brain function. Encephalitis can be caused by
direct infection by bacteria, fungi, viruses, parasites, or immune factors,
which typically occur post-infection. HSV encephalitis is the most common
cause of viral encephalitis and is associated with high mortality and is the
focus of this section.
Background
Epidemiology
 HSV encephalitis is the most likely viral encephalitis to cause fatalities.

o The annual incidence of HSV encephalitis worldwide is 1-4 cases per
1,000,000.
o 90% of cases are HSV-1, and ~7% of cases are HSV-2.
o Mortality is thought to be in the 20-30% range with appropriate
treatment, and above 50% without treatment.
Pathophysiology
 How HSV enters the central nervous system is not fully understood, nor is it
known if acute encephalitis is the result of a primary infection or
reactivation of a latent infection.
o HSV is transmitted to humans through mucous membranes or through
damaged skin and then infects sensory neurons. It can live dormant in
the nerves and then become reactivated.
 There are no pathognomonic signs or symptoms for HSV encephalitis.

 Common symptoms include confusion (90%), fever (90%), headache,
nausea and vomiting (30%), and focal neurologic symptoms (20-40%).
 Levels of consciousness can range from alert at presentation, to drowsy, to
coma.
 Seizure (both focal and general) will occur in approximately 40% of patients
with HSV encephalitis. A small percentage (~10%) will develop status
epilepticus.
 Blood tests will not confirm the diagnosis of HSV encephalitis but may be
useful to rule out other diagnoses on the differential.
o A normal white blood cell count can be found in patients with HSV
encephalitis.
 CSF analysis is necessary if encephalitis is suspected. HSV encephalitis will
typically have increased lymphocytes, normal to mildly elevated glucose,
and normal to mildly elevated protein; 5% of cases will have normal CSF.
 PCR detection of the HSV DNA is the gold standard for diagnosis. The test
has a high sensitivity (95%) and specificity (99%); however, false negatives
can occur, particularly in the first few days.
 MRI typically reveals hyperintense signals (on T2/FLAIR sequences) of the
medial temporal, inferior frontal, and insular regions.
Medical Management
 IV acyclovir is an effective treatment for HSV encephalitis and is associated

with decreased mortality at 6 mo.
o Dosing is 10 mg/kg every 8 h for 14-21 d but needs adjustment in
patients with renal impairment.
o Treatment should be started as soon as the diagnosis is suspected.
 There is insufficient evidence to recommend steroid use as an adjuvant
therapy.
 Antiepileptics for seizure prophylaxis are commonly used, though there is
no established recommendations to support such practice. When seizures do
occur, they should be treated aggressively.
o Continuous EEG monitoring should be obtained in patients with
fluctuating mental status to rule out subclinical status epilepticus.
 Major complications include seizures, status epilepticus, and brain swelling
with the potential for herniation, which is the most concerning complication.
 Patients often require ICU monitoring.
Prognosis
 As stated previously, mortality is thought to be in the 20-30% range with

appropriate treatment and above 50% without treatment.
 Residual neuropsychiatric deficits are common.
 Worse outcome is associated with delayed initiation of acyclovir, older age,
coma, and restricted diffusion in MRI.
 See chapter: Central Nervous System Infection
Cervical Artery Dissection
 Cervical artery dissection (CeAD) refers to the dissection of either the

vertebral artery or the internal carotid artery and accounts for ~2% of all
ischemic strokes. It is an important cause of stroke, particularly in the
young. It is a diagnosis that should not be missed.
Background
Epidemiology
 CeAD includes both carotid artery dissection (CAD) and vertebral artery
dissection (VAD) and is thought to be the cause of approximately 2% of all
strokes and up to 24% of strokes in children and young adults.
 The mean age of occurrence is 44, and CeAD is rare after 65. It is slightly
more common in men.
 Dissection is considered to be either “extracranial” or “intracranial”, with
extracranial dissection being more common.
 Risk factors include connective tissue disease, hypertension, and history of
trauma. Ultimately, the cause of CeAD is thought to be multifactorial.
Pathophysiology
 CeAD results in a separation of vessel wall layers, creating a false lumen

which then fills with blood, leading to vessel wall hematoma formation and
thrombus.
 The vessel wall hematoma narrows the lumen, which can result in decreased
blood flow and possible occlusion of the vessel. Mass effect on surrounding
structures can also result.
 While hypoperfusion from the decreased size of the true lumen can result in
ischemic stroke, thromboembolism is the more common cause of stroke in
CeAD.
Clinical presentation
 While spontaneous dissections do occur, both CAD and VAD are often
associated with preceding cervical trauma, such as vigorous physical
activity, chiropractic manipulation, and more benign movements such as
sneezing and coughing.
 Symptoms:
o Headache and neck pain are the most common symptoms, occurring
in nearly 80% of patients.
o Neurologic deficits such as Horner’s syndrome, tinnitus, and facial
pain are concerning for internal CAD, whereas vertigo or ataxia are
more concerning for VAD.
o Local symptoms (ie, pain) typically occur within minutes to hours
after the dissection, and a subsequent ischemic event may occur.
Delayed onset of neurologic symptoms can take up to 1 mo.
 A cochrane review in 2009 determined that MRA and/or CTA of the neck
are appropriate imaging modalities to order if concerned for CeAD.
 U/S is limited due to its inability to visualize above the mandible and its
poor diagnostic value for intracranial dissections.
 Routine labs such as CBC, metabolic panel, and coagulation studies should
be ordered in patients with suspected CeAD.
 Treatment goals are to save at-risk brain tissue and prevent stroke.
 Medical Management
o Antiplatelet or antithrombotic agents are reasonable choices, as no
evidence to date has demonstrated one therapy to be superior to the
other. Patients may require procedural therapy when persistent or
recurrent symptoms occur despite anticoagulation.
o CeAD without aortic dissection is not a contraindication for tPA in
patients with ischemic stroke. This should be discussed with the
neurology team.
 See chapter: Cervical Artery Dissection
 Cervical Artery Dissection
Posterior Reversible Encephalopathy Syndrome
 Posterior reversible encephalopathy syndrome (aka posterior

leukoencephalopathy syndrome) is a clinical syndrome that is diagnosed
using neuroimaging in a particular clinical context, such as in hypertensive
encephalopathy, eclampsia, renal disease, and the use of cytotoxic drugs.
These patients can present with acute neurological symptoms, such as
headache, altered mental status, seizure, and vision change. Neuroimaging
typically reveals vasogenic edema in the bilateral parieto-occipital regions.
Background
Epidemiology
 Though increasingly common, statistics on incidence are unknown.

o PRES has been reported in all age groups but is most common in
middle-aged individuals and occurs more commonly in females.
 Conditions associated with PRES include renal disease (55% of patients
have renal disease), sepsis, immunosuppressive therapy (particularly
cyclosporine and tacrolimus are known to be triggers), and autoimmune
disorders (50% of PRES patients have autoimmune disorders).
Pathophysiology
 The pathophysiology of PRES is under study but is believed to be caused by

endothelial injury or dysfunction leading to breakdown of the blood-brain
barrier resulting in brain edema. This dysfunction is thought to be due to
either:
o Rapid blood pressure fluctuations (rise and or fall) leading to vascular
leakage and vasogenic edema (significantly elevated blood pressure is
observed in approximately 70% of cases; however, it has also been
known to occur in septic and hypotensive patients).
o Toxins (either exogenous or endogenous) destroying the endothelium,
resulting in leakage, edema, and vasospasm (this theory is supported
by the occurrence in septic, immunosuppressed patients, or patients
with autoimmune disorders).
 Though there are no clearly defined criteria for the diagnosis of PRES,
Fischer et al. proposed the following:
o Acute onset of neurologic symptoms
o Vasogenic edema on neuroimaging
o Reversibility of clinical and/or radiologic findings
Clinical Presentation:
 Symptoms may develop over hours to days:

o Headache is usually dull, diffuse, and gradual in onset and present in
approximately 50% of patients.
o Encephalopathy is observed in 80% of patients and can present with a
range of symptoms, such as confusion and coma.
o Tonic clonic seizures occur in 60-75% of patients.
 Status epilepticus (5-15% of patients) is one of the most severe
complications.
o Vision changes are reported in approximately 30% of patients.
o A focal neurologic deficit is present in approximately 5-15% of
patients.
 MRI is the diagnostic test of choice, and findings consistent with PRES
include vasogenic edema, often found in the parieto-occipital locations
bilaterally.
 An LP should be performed to rule out other causes of encephalopathy if
there is suspicion for meningitis or encephalitis. No CSF findings specific
for PRES have been determined.
 Magnesium levels are reduced in a significant percentage of PRES patients.
Treatment
 Treatment for PRES is supportive.

 Treat an underlying cause if determined. If an offending
medication (immunosuppressive or cytotoxic medications) is identified, it
should be stopped or tapered.
 Management of blood pressure is the mainstay of treatment. A reduction in
blood pressure levels by 25% is recommended, and strict hemodynamic
monitoring should be achieved to avoid fluctuations in blood pressure. No
specific antihypertensive agent is recommended over another, but an easily
titratable medication is desirable. Caution should be used when lowering
blood pressure in patients who are only slightly hypertensive (130-140 mm
Hg).
 Administer anticonvulsant medications to those who seize. There is
insufficient evidence to suggest prophylactic seizure medications.
 Magnesium is known to have anticonvulsant effects and vasodilating effects
and should be maintained within a normal range.
 ICU monitoring may be necessary for blood pressure control or
complications such as status epilepticus or ICH.
Prognosis
 Most patients recover fully, though recurrent seizures have been reported.
Radiologic improvement also occurs in most cases.
 5-10% of patients will have a recurrent episode. This is more common in
patients with uncontrolled blood pressure.
Cerebral Venous Thrombosis
 Cerebral Venous Thrombosis (CVT) is a thrombosis of the dural

sinus and/or cerebral veins. It is a rare condition that is challenging to
diagnose due to the multitude of risk factors and various presentations
depending on the location of thrombosis. However, headache is the most
common presenting symptom.
Background
Epidemiology
 CVT is an uncommon cause of stroke that affects 1.3 per 100,000 annually.
It accounts for 0.5-1% of all strokes and primarily affects young people and
women of childbearing age.
 Approximately 2% of pregnancy-associated strokes are attributed to CVT.
 Risk factors include those that are classically linked to venous thrombosis.
They can be both acquired (surgery, trauma, pregnancy, post-partum,
antiphospholipid syndrome, cancer, exogenous hormones, etc) and genetic
(factor 5 leiden, antithrombin III, protein C, protein S, etc).
 Infections in the parameningeal locations (ear, sinus, mouth, face, neck)
have also been linked to CVT, though more commonly in children.
Pathophysiology
 The cerebral sinuses provide a system through which blood from the brain
can drain into the internal jugular veins. Additionally, CSF is transported
from the subarachnoid space to the venous system via the arachnoid
granulations. Blocking of this CSF transport results in intracranial
hypertension.
 Cortical veins that drain blood from brain tissue into the cerebral sinuses can
be obstructed and cause an increase in venous and capillary pressure,
leading to a breakdown of the blood-brain barrier and subsequent edema and
potentially brain tissue damage.
 Headache is the most common presenting symptom of CVT (90%) and may
be the only symptom in 25% of patients. It most commonly presents over
days to weeks, although it is well documented that patients with CVT may
present with a “thunderclap headache”.
 Clinical manifestations of CVT are variable and depend on the location of
occlusion. While the symptoms may be variable, a few syndromes have
been discussed in the literature:
o Isolated intracranial hypertension syndrome (headache, papilledema,
visual problems).
o Stroke secondary to venous infarct resulting in a focal syndrome
(focal deficits, seizures, or both).
o Encephalopathy (mental status changes, coma).
 Approximately 40% of patients will experience seizures.
 CBC, complete metabolic count, PT, and PTT are recommended in a patient
with suspected CVT by the AHA/ASA.
 D-dimer is a study of considerable interest with CVT. Per the 2011
AHA/ASA statement on the diagnosis and management of CVT, a normal
d-dimer may help identify patients with low probability of CVT but does not
rule it out.
 There are no specific CSF abnormalities in CVT.
 30-50% of patients with CVT are found to have concomitant ICH.
 MRI+MRV is preferred over CT+CTV due to its higher sensitivity.
However, if MRI is not available, CT+CTV is the appropriate initial study.
Treatment
 Therapy is aimed at treating the underlying cause and symptoms, the
prevention of complications, and most often, providing anticoagulation.
o Consult Neurology upon making the diagnosis. Depending on the
severity, initial management may require a stroke unit or ICU to
optimize care and minimize complications.
o Adjusted dose unfractionated heparin or low molecular weight
heparin is the treatment of choice in the case of CVT, irrespective of
the presence of ICH at the time of CVT diagnosis.
o Currently, endovascular treatment and decompressive surgery are not
recommended in routine cases.
Prognosis
 The mortality of CVT is thought to be 5-10% and decreasing (thought to be

due to the identification of less severe cases).
 80% of patients recover without functional disability but may have chronic
symptoms such as headache and fatigue.
Preeclampsia with severe features
 Preeclampsia is a serious pregnancy-related condition affecting 3-5% of

pregnancies. It is a spectrum of disease ranging from mild to severe. The
diagnosis is made after 20 weeks of gestational age or up to 6 weeks
postpartum in patients with hypertension and evidence of organ dysfunction,
as noted below. New-onset headache not improved with acetaminophen and
not accounted for by an alternative diagnosis qualifies as a severe feature of
preeclampsia.
Background
Definition
 The diagnostic criteria for preeclampsia were changed in 2013 by the

American College of Obstetricians and Gynecologists (ACOG) and in 2014
by the International Society for the Study of Hypertension in Pregnancy
(ISSHP). Both organizations removed proteinuria as a requirement for
diagnosis. Proteinuria and elevated blood pressure still qualifies; however,
other criteria can be substituted for the proteinuria.
 Eclampsia is defined as preeclampsia with a generalized clonic-tonic seizure
when no other cause of seizure is determined. It is often, but not always,
preceded by headache and other neurologic symptoms. In randomized
controlled studies, eclampsia ultimately develops in 1.9% of patients with
preeclampsia and 3.2% of patients with severe preeclampsia.
Epidemiology
 Based on literature reviews, 4.6% of pregnancies worldwide and 2.3-3.4%
of pregnancies in the U.S. are affected by preeclampsia.
 Risk factors include previous preeclampsia or hypertension in pregnancy,
diabetes, kidney disease, autoimmune disorders such as lupus and
antiphospholipid disorder, first pregnancy, age >40, polycystic ovarian
syndrome, and 10 years between pregnancies.
Pathophysiology
 The pathophysiology is not completely understood and is thought to involve

both fetal/placental factors. Please refer to the appropriate OB chapters for
further discussion.
 Preeclampsia should be considered in any ED patients with a gestational age

>20 weeks OR up to 6 weeks post-partum who meet the blood pressure
criteria of diagnostic criteria for preeclampsia severe features with a
complaint of a significant headache or visual disturbance.
o Most diagnoses of preeclampsia are made in the clinic during routine
antenatal care when the patient is asymptomatic.
 No specific imaging is recommended. If pulmonary edema was suspected by

history and physical, lung imaging is recommended.
 When preeclampsia is considered on the differential diagnosis, a CBC
(thrombocytopenia is a criterion for diagnosis), metabolic panel including
renal and hepatic function tests, and a urine analysis should be obtained.
Therapeutic considerations
Medical management
 The only cure for preeclampsia is delivery of the placenta. Generally, this is
indicated in pre-eclamptic patients with severe features >34 weeks of
gestation.
 Consult the Obstetrics service if there is concern that the patient may have
preeclampsia with severe features, as they can assist with risk assessment,
surveillance of the mother and fetus, and help guide the management of
hypertension and end organ complications.
 Patients with preeclampsia with severe features should be managed as
inpatients.
o If severe hypertension is confirmed as persistent (15 min or more),
antihypertensive therapy should be started as soon as possible.
Nifedipine, hydralazine, and labetalol are all appropriate agents, with
none demonstrating superiority over the others. Initial dosing
recommendations from ACOG are listed below:
 Nifedipine 10-20 mg orally initial dose
 Hydralazine 5 mg IV initial dose
 Labetalol 10-20 mg IV initial dose
o Seizure prophylaxis with magnesium sulfate (MgSO4) is
recommended for preeclamptic patients with severe features.
MgSO4 is used intrapartum (typically started at induction or at the
onset of labor) and/or postpartum. MgSO4 is not typically used in the
antepartum period. Dosing is 4 g IV over 5 min followed by 1 g/h IV.
o For headache management, the MgSO4 utilized for seizure
prophylaxis may help relieve some of the pain.
 Acetaminophen 650-1000 mg is safe.
 Metoclopramide 10 mg is the next-line treatment option.
Prognosis
 Preeclampsia and eclampsia are associated with 10-15% of maternal deaths

worldwide and represent the 4th leading cause of pregnancy-related deaths
in the U.S.
 Preeclampsia is known to cause intrauterine growth restriction,
oligohydramnios, and preterm birth, all of which increase the risk of
perinatal morbidity and mortality.
 See chapter: Emergencies After 20 Weeks Gestation
Idiopathic Intracranial Hypertension
 Idiopathic intracranial hypertension (IIH), formerly known as pseudotumor

cerebri, is a disorder that results in increased intracranial pressure (ICP) with
the corresponding symptoms (headache and visual change) and no cause of
increased ICP on imaging as well as normal cerebrospinal fluid studies.
While for many patients these symptoms will wax and wane for weeks,
months, or even years, patients with rapid or significant vision loss are of
most concern in the emergency setting.
Background
Epidemiology
 The frequency of IIH is thought to be approximately 1 case per 100,000 per

year, though frequency is increasing with the obesity epidemic.
 IIH primarily affects women of childbearing age with obesity.
Pathophysiology
 The exact pathophysiology is unclear, but the proposed theories are based
on either increased production or decreased absorption of the CSF.
 History
o Headache is the most common symptom, affecting 84%.
 This is usually moderate to severe, and worse upon waking.
o Visual Changes
 ~70% of patients experience transient visual obscurations.
 Patients may report double vision (~33%). This is most often
the result of a 6th cranial nerve palsy causing a horizontal
diplopia.
o Other common symptoms include back pain and tinnitus (~60%).
o Physical Exam
 A fundoscopic exam must be performed if IIH is suspected.
Papilledema on exam is the hallmark finding and is typically
bilateral and symmetric. Unilateral papilledema can be seen in
a small percentage of patients.
 There is an association between high-grade papilledema
and vision loss, and the severity of papilledema
influences the treatment strategy.
 If papilledema is discovered, the following must be performed:
 Visual acuity check
 Formal visual fields check
 Dilated fundoscopy
 Check blood pressures to exclude malignant
hypertension (diastolic >120 mm Hg, or systolic >180
mm Hg)
 If papilledema is discovered, brain imaging is necessary within 24 h and

ideally sooner to rule out other causes of papilledema.
o The preferred imaging study in suspected IIH patients is MRI,
specifically with contrast if there is concern for an intraparenchymal
lesion or meningeal process causing increased intracranial pressure.
o If MRI is not available, a CT with contrast is recommended.
o Additionally, a venogram (MR or CT) is an essential part of the
work-up to exclude venous sinus thrombosis as a cause of
papilledema.
o Features on neuroimaging suggestive of increased intracranial
pressure may or may not be seen (ie, enlarged optic nerve sheath,
tortuosity of optic nerve, flattened posterior globe, empty sella).
These are not pathognomonic for IIH, and their absence does not
exclude it.
 CSF analysis is necessary for the diagnosis, and the opening pressure must
be measured.
o An opening pressure >250 mm is the threshold for diagnosis. This
should be measured in the lateral decubitus position with the legs
relaxed.
 It is worth noting that the patient’s pain or nervousness causing
Valsalva maneuvers will increase the pressure. Anxiolytics can
be considered on an individual basis.
o The CSF should be sent for glucose, protein, cell count, and cultures.
 CSF analysis should be normal in cases of IIH.
 Preserving vision is the ultimate goal along with alleviating symptoms

(headache). Medical and surgical treatments are used based on the degree of
visual impairment, the rate at which it occurred, and the availability of
specialists.
 Medical Management
o Acute management depends on symptoms.
 Those with precipitous visual decline will need surgical
management (potentially a ventriculoperitoneal shunt).
 If symptoms appear to be worsening at an alarmingly
fast pace or new vision loss has occurred, a discussion
with Neurology is warranted.
 A recommendation for IV steroids or serial lumbar
punctures may be made by a consulting service as a
temporary measure. However, serial LPs are not
recommended in the long-term management of IIH.
 Patients with a known diagnosis of IIH with an
exacerbation of headache without red flag symptoms
(SNOOP2) or papilledema do not need neuroimaging or
repeat lumbar puncture.
 Long-term management includes weight loss, salt and fluid
restriction, and in some cases medications such as
acetazolamide (most commonly prescribed initial medication
for IIH, with typical starting dose 250-500 mg twice per day),
topiramate, or furosemide.
 These medications are recommended to be prescribed in
conjunction with Neurology or primary care for
appropriate education, dosing, and monitoring of side
effects.
 A 2015 Cochrane review determined that there is
insufficient evidence regarding the efficacy of
acetazolamide. More research is necessary.
 Headaches can be managed using typical migraine treatment
protocols (tailored to the individual patient and the
circumstance, eg, pregnancy, allergies).
Prognosis
 Vision loss is the major morbidity in IIH.

 IIH is a chronic condition, and patients diagnosed with this condition have
been known to have higher rates of anxiety and depression and a lower
quality of life.
Giant Cell Arteritis
 Giant cell arteritis (GCA) is a large and medium vessel vasculitis that can
present with headache with the potential complication of vision loss.
Background
Epidemiology
 GCA is an uncommon diagnosis, with an annual incidence of 20 per

100,000 at risk.
 GCA is more common in females than males (2-3 : 1), is more prevalent in
the Northern European population, and is found in patients older than 50 y
(though a few cases of younger diagnosis have been published).
 30-50% of patients with GCA also have polymyalgia rheumatica, which is
characterized by morning stiffness in the neck, pelvic girdle, and proximal
upper extremities.
Pathophysiology
 GCA is an idiopathic vasculitis of the medium and large vessels that most
commonly affects the aortic arch but often involves branches of the carotid
arteries.
 GCA was formerly referred to as “temporal arteritis” or “cranial arteritis;”
however, these terms are now less emphasized as they understate the
involvement of other vessels that ultimately affect diagnosis and prognosis.
 Molecular studies have suggested that arterial wall remodeling and intimal
hyperplasia occur as a result of immune response networks activating a
number of cytokines and inflammatory mediators.
Diagnostic criteria
 The diagnosis of GCA is made based on a combination of physical exam
findings, symptoms, blood work, and biopsy findings.
o Temporal artery biopsy remains the gold standard for diagnosis.
 The 1990 ACR classification criteria are listed in Criteria for the
Classification of Giant Cell Arteritis
o When 3 of the 5 criteria in Criteria for the Classification of Giant
Cell Arteritis were met, a diagnosis of GCA was made with a
sensitivity of 93.5% and specificity of 91.2%.
 Of note, GCA has two phenotypes: cranial GCA or extracranial GCA; these
are often referred to as large vessel GCA. Cranial GCA is the phenotype that
more often presents with headache and/or vision change.
 Presentation varies, but patients often present with headache (30-80%), low
grade fever (20-50%), scalp and/or temporal artery tenderness (40-70%),
jaw pain (30-70%), and potential monocular or binocular vision loss (12-
40%).
 Most patients will have a markedly elevated ESR or CRP (89.8% in one
study); however, other studies have shown that 24% of biopsy-proven GCA
had a normal ESR. Thus, ESR and CRP are imperfect markers of GCA;
additionally, if they are normal, GCA is not excluded.
 Ultrasound and MRI of the temporal artery have not become the standard of
care but are currently being studied as a means of diagnosis.
Biopsy Evaluation
 The gold standard for diagnosis is temporal artery biopsy. However, given
the risk of vision loss, steroid treatment should not be withheld before the
biopsy. Use of steroids does not seem to decrease the rate of positive
findings.
 Temporal artery biopsy should be pursued in all patients suspected of having
GCA.
Medical Management
 Treatment of suspected GCA should never be deferred until biopsy, as it is

rapidly effective and usually prevents vision loss.
 Prednisone 40-60 mg/d or 1 mg/kg is the typical dose and administered for
2-4 weeks with a taper to be followed afterwards.
 1000 mg/d for 3 d has been used in patients with vision loss.
 Urgent Ophthalmology consultation is necessary for patients with vision
loss and concern for GCA.
 While still being elucidated, it is recommended that patients with GCA with
no contraindications receive low-dose aspirin to reduce the risk of cerebral,
ocular, and cardiovascular events.
 Patients should have a close follow up with their primary care physician as
well as a referral to Rheumatology.
Prognosis
 The most feared complications include vision loss and aortic aneurysm
rupture or dissection.
 In the absence of aggressive treatment within 24 h, the likelihood of
restoring functional vision is very low.
 GCA is associated with increased risk of myocardial infarction, stroke, and
peripheral vascular disease within the first month after diagnosis.
 See chapter: Aortic Dissection
 See chapter: Abdominal Aortic Aneurysm
Acute Angle Closure Glaucoma
 Acute angle closure glaucoma (AACG) is an eye-threatening condition that

typically presents with eye pain and vision change. It is often accompanied
by headache. Immediate treatment is essential and required to prevent vision
loss.
Background
Epidemiology
 Glaucoma is the second-leading cause of blindness in the world. Nearly 70

million people in the world between the ages of 40-80 years suffer from
acute angle glaucoma, with the highest prevalence in those of Asian descent.
 Risk factors for acute angle-closure glaucoma include family history, age
over 60, female, farsighted, various medications, and East Asian descent.
Pathophysiology
 The ciliary body creates aqueous humor, which flows through the pupil to
reach the anterior chamber and exits the eye. The balance of production and
drainage determines the intraocular pressure. A condition called “pupillary
block” occurs when the aqueous humor cannot flow through the pupil,
resulting in pressure building up behind the iris. This results in pain and may
lead to decreased vision.
Precipitants
 Dim light (classic case of walking into a movie theater), medications
(mydriatics, anticholinergics, sulfa derivatives), accommodation (eg,
reading).
 History
o Patients may present with headache, blurred vision, eye pain, and
“halos” around lights. They may also report nausea and vomiting.
 Physical Exam
o Exam may demonstrate a mid-dilated (4-6 mm) pupil that is
asymmetric or oval. The pupil may be sluggish or non-reactive to
light.
 Exam may also demonstrate intraocular pressure (IOP) greater
than 30 mm Hg (normal IOP is not higher than 21 mm Hg).
 Perform a fundoscopic exam to search for optic nerve
cupping, as this will indicate the need for more urgent
treatment.
 Be sure to examine both eyes.
 Renal function and electrolytes should be checked in patients who are of

concern for AACG, as carbonic anhydrase inhibitors and osmotic agents
may be used as therapeutic agents.
 No radiographic studies are recommended in cases of suspected AACG.
Medical Management
 The aim is to lower IOP and help alleviate symptoms.

o Medications
 Topical B-blocker (eg, timolol 0.5%, caution with asthma or
COPD), alpha-2 agonist (eg, brimonidine 0.1%), prostaglandin
analog (eg, latanoprost 0.005%), and carbonic anhydrase
inhibitor (eg, dorzolamide 2%) should be initiated
immediately. Three rounds of these medications may be given,
with each round separated by 15 min.
 Recheck IOP in 1 h.
 Systemic carbonic anhydrase inhibitors (eg, acetazolamide
250-500 mg IV or 250 mg x 2 PO can be given if no IV) if
topical agents did not resolve IOP.
 If IOP does not decrease at this point, repeat topical
medications and give osmotic agent (eg, mannitol 1-2 g/kg IV
over 45 min).
 This is contraindicated in CHF, renal disease, and
intracranial bleeds.
o Urgent Ophthalmology consult should be made.
 Discuss goal of IOP decrease with Ophthalmology.
Prognosis
 The other eye should be evaluated by an ophthalmologist, as up to 50% of

the “fellow” eyes suffer from AACG within 5 years.
 Patients should be instructed to tell their first-degree relatives to get
screened, as they may have occludable angles.
For more information, check out:
 Glaucoma
 See chapter: Glaucoma
Carbon Monoxide Poisoning
 Carbon monoxide (CO) is an odorless, tasteless, colorless gas that binds

hemoglobin with a much greater affinity than oxygen and forms
carboxyhemoglobin (COHb). As a result, tissue oxygen delivery is
impaired, and an inflammatory cascade can lead to neurologic symptoms
and potentially death. The most common initial presenting symptom is
headache.
Background
Epidemiology
 CO poisoning causes approximately 50,000 ED visits per year, of which an

estimated 21,000 are non-fire-related unintentional exposures. Non-fire CO
poisoning results in 1,200 deaths per year.
 Sources of CO include fires, inappropriately functioning furnaces, motor
vehicles in poorly ventilated areas (ie, garages), and poorly ventilated fuel-
burning devices, such as charcoal grills, kerosene stoves, heaters, and gas-
powered generators.
 All humans have a small amount of CO in the body. A normal
carboxyhemoglobin level is 2-3%, while smokers can have levels of
approximately 10-15%.
Pathophysiology
 CO binds the four sites of the hemoglobin molecule at 200-250 times higher
affinity than oxygen. Additionally, the oxygen-hemoglobin dissociation
curve is shifted leftward, further impairing the delivery of oxygen to the
tissues.
 The COHb level depends on the length of exposure and concentration of CO
in the surrounding area.
 CO also impairs mitochondrial function, ultimately resulting in an
inflammatory cascade leading to oxidative stress and free radicals,
worsening tissue hypoxia.
 Consider this diagnosis particularly if family and pets have similar

symptoms or if the patient has an occupation that puts them at risk (ie, work
with motorized vehicles in enclosed spaces).
 Headache is the most common presenting symptom of CO exposure, but the
description and intensity do not correlate with COHb levels.
 Flu-like presentation is common (headache, nausea, vomiting, dizziness, and
muscle aches), but patients can report more severe symptoms such as chest
pain, shortness of breath, confusion, syncope, seizure, or even coma.
 The cherry red skin that has classically been taught is uncommon in clinical
practice.
 Cyanide toxicity MUST also be considered in cases following smoke
inhalation.
 A COHb should be measured off of either a venous or arterial blood

sample. Note that a carboxyhemoglobin measurement may need to be
requested specifically!
o Standard pulse oximetry cannot screen for CO exposure, as it cannot
differentiate between oxyhemoglobin and carboxyhemoglobin.
o A non-invasive pulse co-oximeter for COHb levels is not sufficiently
accurate to diagnose CO toxicity.
 If a patient has moderate to severe CO poisoning (as evidenced by syncope,
ataxia, dyspnea, chest pain, rhabdomyolysis, arrhythmias, pulmonary
edema, seizure, or coma), it is recommended that ECG and cardiac
biomarkers be obtained to identify cardiac injury and predict poor outcome.
Medical Management
 If there is concern about CO poisoning, start treating with 100% oxygen via
non-rebreather mask to minimize the chance of neurological sequelae.
o The half-life of COHb is 4-6 h. This decreases to 1 h if a patient is
placed on a non-rebreather with 100% oxygen. With hyperbaric
oxygen at 2.8 atm, the half-life decreases to 20-30 min.
 If patients have an elevated COHb level and report symptoms consistent
with CO toxicity, call thePoison Control Center (1-800-222-1222) for
guidance.
 It is unclear who will benefit from hyperbaric oxygen. A 2017 ACEP
clinical policy statement indicates that it remains unclear whether hyperbaric
therapy is superior to normobaric oxygen therapy for neurocognitive
outcomes. Traditionally, indications for hyperbaric treatment have included:
o COHb level >25%
o Pregnant with a level >15% (this has been the recommendation
because fetal hemoglobin binds COHb, but the data are limited)
o Cerebellar symptoms or focal neurologic deficits
o Other suggested indications include loss of consciousness, coma,
seizure, ongoing altered mental status, ongoing headache complaints,
greater than 36 years of age, or prolonged exposure
 What does hyperbaric oxygen do?
 Beyond decreasing half life, it decreases the
inflammatory cascade and reperfusion injury
 Patients should be treated until their COHb level is <10% and their
symptoms have resolved.
 Discuss the patient with Cardiology If the troponin is elevated, there are
EKG changes, or if the patient has persistent chest pain.
 Make sure that the gas company is contacted to check the levels in the
building!
Prognosis
 The existing evidence does not clearly determine who is at risk for delayed
neuropsychiatric sequelae. Patients may show cognitive effects weeks to
months after toxicity.
 There is evidence to suggest that CO poisoning may be linked to an
increased risk of death from myocardial infarction.
For more information:
 EM:RAP Audio
 See chapter: Carbon Monoxide Poisoning
 See chapter: Cyanide
 See chapter: Methemoglobinemia
Pituitary Apoplexy
 Pituitary apoplexy is a rare but life-threatening condition that results from
infarction or hemorrhage of the pituitary gland and most often presents with
a sudden and severe onset headache and visual changes.
Background
Epidemiology
 6.2 cases per 100,000, with an incidence of 0.17 per 100,000.

 It is most commonly associated with pituitary adenomas or microadenomas,
although it can occur in normal pituitary glands (after postpartum
hemorrhage called Sheehan’s syndrome).
 Precipitating factors are present in 40% of the following cases: surgical or
angiographic procedures, head trauma, pregnancy, anticoagulant use, or
hormonal treatment that leads to pituitary stimulation.
Pathophysiology
 Pituitary apoplexy is the result of infarction or hemorrhage of the pituitary

gland. The pathophysiology is not completely understood.
 Patients with pituitary apoplexy have various presentations depending on the

extent of the hemorrhage.
 80% report headache (often described as thunderclap in onset); 50% report
vision change, and roughly the same percentage have oculomotor palsies.
Other common symptoms include photophobia, nausea, vomiting, and
altered level of consciousness. A small percentage present with coma.
 CT without contrast is often the initial image acquired in the ED, but CT is
reportedly only diagnostic in 21-28% of pituitary apoplexy cases.
 MRI is the preferred study and can confirm the diagnosis in over 90% of
cases.
 All patients with pituitary apoplexy should have serum testing for CBC,
electrolytes, renal and liver function, coagulation, and pituitary function
(serum cortisol and thyroid hormones).
Management
 Traditionally, management was surgical, although a more conservative
medical approach is becoming more common.
o Contact Neurosurgery as soon as the diagnosis is suspected on
imaging. Surgery is often indicated for those with visual deficits or
altered cognition.
o Contact Endocrinology for consultation.
o If available, contact a neuro-ophthalmologist if the patient has visual
issues.
 Begin empiric IV corticosteroid replacement (eg, hydrocortisone 100-200
mg IV bolus followed by 2-4 mg/h by infusion or 50-100 mg q6h IM
injection) in any patient with acute pituitary apoplexy with hemodynamic
instability, altered mental status, visual field deficits, or reduced visual
acuity.
 If emergency surgery is not required, consider ICU placement, as clinical
status can deteriorate quickly.
Prognosis
 There is no robust evidence to suggest a difference in mortality rates

between surgical vs. medical management.
 Most studies suggest that patients will remain on replacement therapy for
hypopituitarism irrespective of surgical or conservative medical
management.
Benign causes of acute headache
 Primary headaches are classified as (1) migraine, (2) tension-type, (3)

trigeminal autonomic cephalgias, or (4) other. Of these primary headaches,
tension type headache is the most common in the general population, while
migraine is the most common headache diagnosed in the ED. Trigeminal
autonomic cephalgias are a group of headaches that are unilateral and with
autonomic features, and cluster headache is the most common in this
category. Migraine, tension-type, and cluster headaches are discussed in
further detail below.
Background- Tension-type Headache (TTH)
 The term “tension-type headache” replaces previous terms such as a “stress

headache,” “tension headache,” “muscle contraction headache,” and
“ordinary headache.”
 Epidemiology
o Most common headache in the general population, thought to have a
lifetime prevalence of somewhere between 30-78%, but does not
commonly lead patients to present to the ER.
o Studies have indicated that TTH is more common in women than
men, more common in whites, and has a lower prevalence among the
elderly.
 Patients typically present with a bilateral and bandlike headache that is mild
to moderate in intensity.
 The frequency of headaches varies in each patient from less than one
headache per month to nearly every day.
 Pericranial tenderness is the most significant abnormal finding in TTH.
o Detected by manual palpation with rotating movements of fingers
with firm pressure over frontal, temporal, masseter, and other
pericranial muscles.
Medical Management
 Typical treatment involves over-the-counter medications.

o A systematic review concluded that the following were more
effective than placebo:
 Acetaminophen 1000 mg
 Ibuprofen 400 mg
 Ketoprofen 25 mg
o The authors of the same review concluded that the following were
likely more effective than placebo, but the magnitude of effect could
not be estimated based on the current data:
 Aspirin
 Naproxen
 Diclofenac
 NSAIDS (eg, ibuprofen, ketoprofen, naproxen) are less likely to lead to
medication overuse headache than acetaminophen, codeine, and butalbital.
 Combination medications containing caffeine are more effective than
analgesics alone but may cause increased side effects.
 Additional treatment options include chlorpromazine, metoclopramide, and
ketorolac.
Background- Migraine Headache
Epidemiology
 Affects 18% of U.S. women and 9% of U.S. men.

 Migraine headaches are the second most common type of headache in the
general population.
 Migraine is the most commonly diagnosed type of headache in the ED at
nearly 64%.
 Migraine has two major types:

o Migraine without aura:
 Diagnostic criteria for migraine without aura (patients must
meet all criteria)
o Migraine with aura:
 Attacks lasting minutes with reversible visual, sensory, or
nervous system symptoms that are usually followed by
headache or associated migraine symptoms.34
 The fully reversible aura symptoms include:
 Visual (most common, 90% of patients)
 Scintillation (colored lights)
 Scotomas (holes in vision)
 Sensory
 Pins and needles or numbness
 Speech and/or language
 Usually aphasic
 Motor
 Brainstem
 Retinal
 Migraine with aura may occur without meeting the
criteria listed in Diagnostic criteria for migraine
without aura (patients must meet all criteria)
 Migraine with aura may occur without any headache at
all.
 Keep in mind that migraines of either type can cause neurologic and
autonomic features and can appear as strokes! If it looks like a stroke, treat it
like a stroke!
 “POUND” is a popular mnemonic to help remember symptoms consistent
with migraine headache.
 A pregnancy test may be useful to help guide treatment, but laboratory

studies and imaging are generally not indicated.
Medical Management
 Three classes of medications are considered first-line treatment for

migraines: antidopaminergics, triptans, and NSAIDs.
o Antidopaminergics have an unclear mechanism of action but appear
to be effective in treating migraine pain in addition to nausea
symptoms.
 Metoclopramide, prochlorperazine, droperidol, and haloperidol
all have been proven effective, with the first line being either
metoclopramide 10 mg IV or prochlorperazine 10 mg IV.
 Adverse effects of all of these IV antidopaminergics include
akathisia (restlessness and agitation) and other extrapyramidal
symptoms.
 Administering diphenhydramine prophylactically with
prochlorperazine decreases the rates of akathisia.
 Slower rates of infusion also appear to decrease rates of
akathisia.
 Akathisia should be treated with diphenhydramine or
midazolam if it occurs.
 Metoclopramide is the agent of choice in the setting of
pregnancy.
o Triptans are serotonergic receptor agonists, often utilized PO at
home.
 Subcutaneous sumatriptan 6 mg has been shown to relieve
headache in the ED setting.
 Subcutaneous sumatriptan is more likely to be effective in
those who have benefitted from it previously.
 Antidopaminergics have been shown to be more effective in
head-to-head studies.
 Sumatriptan has many adverse effects including flushing, chest
pain, as well as worsening headache or significant headache
recurrence rates.
 Sumatriptan is contraindicated in ischemic heart disease,
uncontrolled hypertension, or peripheral vascular
disease.
o Ketorolac is an NSAID commonly used in conjunction with the
above medications and is generally well tolerated.
 Opioid use in the ED should be discouraged given the addictive properties
and availability of many non-opioid options.
 Opioids are less likely to provide sustained headache relief and lead to
repeated ED visits and medication overuse headache.155
 Dexamethasone decreases the rates of recurrence of severe headache within
72 h of ED discharge. Dexamethasone 10 mg IV is an appropriate dose.
 IV fluids are often used to treat migraines. There is no evidence to suggest
benefit or harm with their use. It would be wise to save their use for those
who appear dehydrated from vomiting.
Background- Cluster Headaches
Epidemiology
 Cluster headaches represent <1% of headaches and affect men more than
women.
 Cluster headaches are the most common form of the trigeminal autonomic
cephalgias and are thought to be autosomal dominant in approximately 5%
of cases.
 Patients generally present with severe unilateral pain near the orbit
accompanied by ipsilateral symptoms such as:
o Conjunctival injection and/or lacrimation
o Nasal congestion and/or rhinorrhea
o Eyelid edema
o Forehead or facial sweating
o Miosis and/or ptosis
 Attacks are known to be so painful that patients may pace the floor and are
unable to lie down.
 Attacks often occur in “clusters” for weeks or months with remission
periods lasting months or years.
 As with other benign headaches, laboratory and radiology studies are not
indicated.
Therapeutic considerations
Medical Management
 Acutely:
o The most effective acute treatment for cluster headache is sumatriptan
6 mg given subcutaneously.
o Sumatriptan is contraindicated in ischemic heart disease, uncontrolled
hypertension, or peripheral vascular disease.
o 100% oxygen given by a high-flow mask with a rate of 12-15
L/min is also highly effective for nearly two-thirds of patients.
Preventative Treatment
 Verapamil is the most widely utilized medication for reducing the frequency
of headaches.
 Lithium and anticonvulsants have also been studied, and new drugs are in
development.
Additional Information
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outline
Chapter PartsChapter Media
 RAPID ACCESS
o Approach to the Critical Patient
o EM:RAP Link
o Key Concepts
o Critical Diagnoses
o Diagnosis
o Disposition
 DEEP DIVE
o Diving into the Can’t Miss Diagnoses
o Subarachnoid Hemorrhage
 Background
 Epidemiology
 Pathophysiology
 Diagnostic considerations
 Clinical presentation
 Decision Rule
 Radiographic and Laboratory Evaluation
 Therapeutic Considerations
o Meningitis
 Background
 Epidemiology
 Pathophysiology
 Meningitis vs Encephalitis
 Diagnostic Considerations
 Clinical Presentation
 Bacterial Meningitis
 Viral meningitis
 Fungal meningitis
o Reversible Cerebral Vasoconstriction Syndrome
 Background
 Epidemiology
 Pathophysiology
 Diagnostic criteria
 Medical Management
 Prognosis
o Viral Encephalitis
 Background
 Epidemiology
 Pathophysiology
 Prognosis
o Cervical Artery Dissection
 Background
 Epidemiology
 Pathophysiology
 Clinical presentation
o Posterior Reversible Encephalopathy Syndrome
 Background
 Epidemiology
 Pathophysiology
 Clinical Presentation:
 Treatment
 Prognosis
o Cerebral Venous Thrombosis
 Background
 Epidemiology
 Pathophysiology
 Treatment
 Prognosis
o Preeclampsia with severe features
 Background
 Definition
 Epidemiology
 Pathophysiology
 Therapeutic considerations
 Medical management
 Prognosis
o Idiopathic Intracranial Hypertension
 Background
 Epidemiology
 Pathophysiology
 Prognosis
o Giant Cell Arteritis
 Background
 Epidemiology
 Pathophysiology
 Diagnostic criteria
 Biopsy Evaluation
 Prognosis
o Acute Angle Closure Glaucoma
 Background
 Epidemiology
 Pathophysiology
 Precipitants
 Prognosis
 For more information, check out:
o Carbon Monoxide Poisoning
 Background
 Epidemiology
 Pathophysiology
 Prognosis
 For more information:
Pituitary Apoplexy
o
 Background
 Epidemiology
 Pathophysiology
 Management
 Prognosis
o Benign causes of acute headache
 Background- Tension-type Headache (TTH)
 Background- Migraine Headache
 Epidemiology
o Therapeutic Considerations
 Background- Cluster Headaches
 Epidemiology
 Therapeutic considerations
 Preventative Treatment
 ADDITIONAL INFORMATION
o References
Table: Critical Diagnoses: The headaches you cannot miss
Diagnosis History/Clinical Testing Management Comments

Findings
Bleeding
Subarachnoi  Thunderclap  CT  Neurosurgic  CT has very
d headache  Lumba al consult high
hemorrhage  Loss of r  Lower blood sensitivity
(SAH) consciousness punctu pressure: within 6
 Neck pain or re Reduction of hours of
stiffness systolic BP headache
Findings
<16020 onset
 Reverse  See Ottawa
anticoagulati Subarachnoid
on Hemorrhage
 Consider Rule
nimodipine
Intracerebral  Headache,  CT  Reverse
hemorrhage usually coagulopath
(ICH) sudden y
 BP control
<140 SBP if
not over 220
when
presenting
 Call
consultants
(Neurosurge
ry /Neuro
ICU) ASAP
 Consider
CTA (CT
angiography
) to assess
for
hemorrhage
expansion
risk 146
Intracranial  Spectrum of  CT  Reverse
hematomas presentations coagulopath
 Epid  Often loss of y
ural consciousness  Contact
hema or coma Neurosurger
toma  Nausea and y ASAP
(ED vomiting
H)  Drowsiness
 Subd and confusion
ural  Seizures
hema  Signs of
toma herniation:
(SD  Ipsilateral
H) pupil dilation
 Cushing
reflex
(hypertension
, bradycardia,
breathing
irregularity)
Findings
Pituitary  Headache  CT  Consult
apoplexy  Vision (not Neurosurger
change (50%) always y
 Often diagno  Consult
postpartum stic) Endocrinolo
 MRI gy
(superi  Hydrocortis
or one 100-200
study) mg IV bolus
initially
Vascular
Cerebral  Neck pain  CTA o  Antiplatelet  Traumatic
artery  Neck trauma r or mechanism
dissection (not always)  MRI/  Antithrombo (40% of the
(CeAD)  Posterior MRA tic agents time)
 Verte stroke preferr  Neurologic
bral symptoms - ed symptoms
arter dizziness, can be
y vertigo, delayed after
disse coordination headache (up
ction (VAD) to 12 hours in
(VA  Anterior VAD and 4
D) stroke days in CAD)
 Carot symptoms -  Can be
id hemiplegia, extracranial
arter slurred or intracranial
y speech,
disse ptosis, miosis
ction (CAD)
(CA
D)
Giant cell  Age >50  CRP  Vision loss:  Start
arteritis  Headache and Methylpredn treatment if
 Jaw ESR isolone 1000 suspicious
claudication (norma mg/day IV  30-50% of
 Vision loss l in 5- for 1-3 days patients also
 Diplopia 30%) in patients suffer from
 Temporal  Tempo with vision polymyalgia
artery ral loss rheumatica
abnormality artery followed by
on exam biopsy PO
prednisone
40 mg/day
 No vision
loss but
suspicion:
40 - 60 mg
Findings
PO
prednisone
with urgent
follow up
 Urgent
Ophthalmol
ogy
consultation
Cerebral  Headache  MRV  Heparin or  Suspect in
venous (absent in or  Low pregnant,
thrombosis 10%)  CTV molecular postpartum,
 Papilledema weight or
 Cranial nerve heparin hypercoagula
deficit (even in ble patients
 Seizure cases of  Variable
ICH) presentations
 Headache can
be acute like
SAH
 A normal d-
dimer does
not rule out
Reversible  Thunderclap  CTA o  Consult  Hemorrhagic
cerebral headache r Neurology if or ischemic
vasoconstric similar to  MRA suspicious stroke will
tion SAH that is  Supportive develop in
syndrome short-lived care 20% of
(RCVS) (minutes to  Discontinue patients
hours) vasoactive  Most frequent
 Occur agents if cause of
multiple possible “thunderclap
times over  ICU headache”
days to weeks necessary in that is not
 Often (80%) severe cases SAH
have a  Multiple
trigger: recurrent
exertion or headaches of
emotion this nature are
suggestive
Ocular
Acute angle  Monocular  Ocular  Initiate the
closure pain acute in pressur following
glaucoma onset e >21 immediately:
 Decreased mm  Topical B-
vision Hg blocker (eg,
 Headache Timolol
 Nausea/ 0.5%)
Findings
vomiting  Alpha-2-
 Eye redness agonist (eg,
 Mid-fixed Brimonidine
dilated pupil 0.1%)
with “steamy  Prostaglandi
cornea” n analog (eg,
Latanoprost
0.005%)
 Carbonic
anhydrase
inhibitors
(eg,
dorzolamide
2%)
 3 rounds q15
min
 Consult
Ophthalmol
ogy
immediately
Idiopathic  Double vision  Fundos  If  Management
intracranial  Flashes of copic precipitous varies with
Hypertensio vision exam vision loss, symptoms and time
n (IIH)  Overweight  MRI contact course of onset
female and Neurology,
 Papilledema venogr as surgery
 CN VI palsy am may be
 Pulsatile (CTV indicated
tinnitus or  Serial
 MRV) lumbar
 Lumba punctures
r (LPs)/IV
punctu steroids
re  Acetazolami
de long-term
(managed by
neurology)
Infectious
Bacterial  Ill appearance Lumbar  Steroids Per Infectious
meningitis  Fever Puncture +/-  IV Disease Society of
 Headache CT (see antibiotics America (IDSA)
 Nuchal comments)  Consider Guidelines, CT
rigidity Cerebrospinal acyclovir if should be obtained in
 Altered fluid (CSF) concerned the following before
mental status studies to for HSV LP:
 Immunocomp order:  Immunocomp
romised  Cell romised
Findings
 Petechiae/ count  CNS disease
purpura  Gram  New onset
 Seizure stain seizure
 Glucos  Altered
e consciousness
 Protein  Focal
 Consid neurologic
er deficit
HSV  papilledema
assays HIV+ /
immunocompromise
d, consider brain
abscess and imaging
with contrast
Viral  Confusion  LP  IV acyclovir Treat with acyclovir
encephalitis  Headache (send 10 mg/kg as soon as this
 Fever for (renally diagnosis is
 Nausea and HSV dosed in suspected
vomiting assays) those with
 Depressed  MRI renal
level of impairment)
consciousness  Treat
 seizure seizures
aggressively
Systemic/Others
Carbon  Confusion,  ABG Oxygen by non- Consider when
monoxide neurologic co- rebreather multiple people
poisoning deficits oximet
Hyperbaric oxygen in same household
 Blurry vision ry chamber for: (including
 Nausea and  Carboxyhem pets) have same
vomiting oglobin symptoms
 Peripheral >25%
cyanosis (pregnant
 Syncope >15%)
 Neurologic
findings
Posterior Elevated blood  MRI  Decrease Check magnesium
reversible pressures MAP by levels
encephalopa Altered level of 25%
thy consciousness  Antiepileptic
syndrome Visual disturbances s typically
(PRES) Seizures required
 May require
ICU
management
Pre- Over 20 weeks  CBC  BP control Eclampsia =
eclampsia gestation or  CMP with preeclampsia +
Findings
postpartum  UA hydralazine tonic-clonic-like
BP >140/90 with 5 mg IV OR seizures
proteinuria labetalol 10
Severe preeclampsia mg IV OR
features: nifedipine
 Thrombocyto 10 mg PO
penia  If seizure
 Renal (eclampsia):
insufficiency IV
 Impaired Magnesium
liver function in 4-6 g load
 Pulmonary IV over 5
edema min and then
 Neurological 1-2 g/h
symptoms:
Headache or
vision change
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AUDIO EM, PC, & UC

VIDEO Courses, Procedures & More

EVENTS Virtual and In-person

Updated: October 9th 2022

The General Approach

 Headache accounts for nearly 3% of all ED visits.

 Critical Diagnoses: The headaches you cannot miss

 Laboratory testing and imaging can provide valuable information when

 Disposition varies depending on facility and resources as well as severity of

Diving into the Can’t Miss Diagnoses

 A more thorough discussion of the data regarding epidemiology, history,

 80% of non-traumatic or spontaneous SAH is caused by an aneurysm

 There is no single history or physical exam finding that significantly

 The Ottawa Subarachnoid Hemorrhage Rule has a sensitivity of 100%

 While in the ED:

 Meningitis can be caused by bacteria, vira, fungi, parasites, or non-

 Patients with meningitis often demonstrate normal brain function; however,

 Headache is present in 27-81% of patients suffering from bacterial

 A patient suspected of having meningitis should undergo an LP, assuming

 Treatment is primarily supportive, as there is no specific antiviral therapy

 Rarely found in patients other than the immunocompromised.

Reversible Cerebral Vasoconstriction Syndrome

 RCVS is the most frequent cause of “thunderclap headache” that is not

 The exact pathophysiology of vasoconstriction is poorly understood but may

 The International Classification of Headache Disorders (ICHD-3) has

 Thunderclap headache (reaches a maximal peak within seconds to minutes)

 If RCVS is suspected based on history, exam, and/or imaging, consult a

 Complications such as SAH, intracerebral hemorrhage (ICH), seizures, or

 Encephalitis refers to inflammation of the brain parenchyma. These patients

 HSV encephalitis is the most likely viral encephalitis to cause fatalities.

 There are no pathognomonic signs or symptoms for HSV encephalitis.

 IV acyclovir is an effective treatment for HSV encephalitis and is associated

 As stated previously, mortality is thought to be in the 20-30% range with

Cervical Artery Dissection

 Cervical artery dissection (CeAD) refers to the dissection of either the

 CeAD results in a separation of vessel wall layers, creating a false lumen

Posterior Reversible Encephalopathy Syndrome

 Posterior reversible encephalopathy syndrome (aka posterior

 Though increasingly common, statistics on incidence are unknown.

 The pathophysiology of PRES is under study but is believed to be caused by

 Symptoms may develop over hours to days:

 Treatment for PRES is supportive.

Cerebral Venous Thrombosis

 Cerebral Venous Thrombosis (CVT) is a thrombosis of the dural

 The mortality of CVT is thought to be 5-10% and decreasing (thought to be

Preeclampsia with severe features

 Preeclampsia is a serious pregnancy-related condition affecting 3-5% of

 The diagnostic criteria for preeclampsia were changed in 2013 by the

 The pathophysiology is not completely understood and is thought to involve

 Preeclampsia should be considered in any ED patients with a gestational age

 No specific imaging is recommended. If pulmonary edema was suspected by

 Preeclampsia and eclampsia are associated with 10-15% of maternal deaths

Idiopathic Intracranial Hypertension

 Idiopathic intracranial hypertension (IIH), formerly known as pseudotumor

 The frequency of IIH is thought to be approximately 1 case per 100,000 per

Radiographic and Laboratory Evaluation