Ebook Diagnostic imaging - Emergency (2nd edition): Part 2

Diagnostic Imaging: Emergency
fragment and the medial condyle of the humerus. This MR was obtained in a 13-year-old baseball pitcher with an acute
injury. (Right) Anteroposterior radiograph shows reduction and screw fixation of the medial epicondyle avulsion fracture
in the same patient.

(Left) Anteroposterior radiograph shows avulsion of the tip of the medial epicondyle
in a 12 year old who started
pitching 3 weeks ago, now with elbow pain and presenting for radiographs. (Right) Coronal T2WI MR in the same patient
shows hyperintense signal throughout the medial epicondyle ossification center. The small osseous fragment could not be
identified. This is an example of Little Leaguer's elbow.

Part II - Nontrauma
Section 1 - Central Nervous System
Introduction to CNS Imaging, Nontrauma
> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Introduction to CNS Imaging, Nontrauma
Introduction to CNS Imaging, Nontrauma
Anne G. Osborn, MD, FACR
Overview
Patients with a number of different nontraumatic disorders of the brain, spine/spinal cord, and head and neck may
present in the emergency department. While virtually any disease in any body part can be seen in the emergency
department, some of the most common urgent entities are discussed in this section.
Nontraumatic Brain Emergencies
Whom to Scan? When to Scan?
Head CT scans in nontraumatized patients with CNS-related complaints are commonly obtained in emergency settings and
account for 70-80% of all CT requests from emergency departments. Prospective studies have revealed that only 8% of
such scans reveal clinically significant abnormalities. Of these cases, over 95% have positive neurologic findings.
Growing concerns about both the costs and the radiation exposure that occurs during CT acquisition have prompted
attempts to identify clinical variables that are independent predictors of abnormal head CT findings in emergency
department patients. Six such clinical variables have been identified:
(1) Age > 70 years
(2) Focal neurologic deficit

(3) Altered mental status
(4) History of malignancy
(5) Nausea &/or vomiting
(6) Derangements in coagulation profile

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Diagnostic Imaging: Emergency
Recent studies do not support the routine use of brain CT in patients under the age of 70 years for the investigation of
uncomplicated headache (i.e., in the absence of additional neurologic findings), migraine-like symptoms, vertigo,
dizziness, drug use, blood pressure abnormality, or generalized symptoms such as fatigue or diffuse weakness.
Presentation at an emergency department with a known patient history of seizure is also not predictive of abnormal head
CT findings.
Nontraumatic Hemorrhage and Vascular Lesions
Spontaneous (i.e., nontraumatic) intracranial hemorrhage and vascular brain disorders are second only to trauma as
neurologic causes of death and disability. When a patient with no history of trauma presents in the emergency
department with sudden onset of a neurologic deficit, NECT scans are the most appropriate initial imaging study.
Challenging questions arise when screening NECT discloses parenchymal hemorrhage. What are the potential causes? Is
the patient at risk for hematoma expansion? Should further emergent imaging be performed?
The most recent American Heart Association/A merican Stroke Association guidelines recommend emergent CT or MR as
the initial screening procedure to distinguish ischemic stroke from nontraumatic intracranial hemorrhage. If the patient is
older than 45 years and has preexisting systemic hypertension, a putaminal, thalamic, or posterior fossa intracranial
hemorrhage is almost always hypertensive in origin and does not require additional imaging.
In contrast, lobar or deep brain bleeds in younger patients or normotensive adults, regardless of age, usually require
further investigation. Contrast-enhanced CT/MR with angiography may be helpful in detecting underlying abnormalities,
such as arteriovenous malformation, neoplasm, and cerebral sinovenous thrombosis.
A CT angiogram (CTA) is indicated in patients with sudden clinical deterioration and a mixed-density parenchymal
hematoma (indicating rapid bleeding or coagulopathy). CTA is also an appropriate next step in children and young/middleaged adults with spontaneous intracranial hemorrhage detected on screening NECT. Likewise, CTA is appropriate in
patients with aneurysmal, perimesencephalic nonaneurysmal, or convexal subarachnoid hemorrhage.

If a CTA is negative, emergency MR is rarely necessary in patients with unexplained “spontaneous” intracranial
hemorrhage (sICH), although a follow-up nonemergent MR with and without contrast can be very useful. Evidence for
prior hemorrhage on T2* sequences (GRE or SWI) can be very helpful in narrowing the differential diagnosis. Multifocal
“black dots” in elderly patients with sICH is typical for chronic hypertensive encephalopathy and amyloid angiopathy
(CAA). Basal ganglia and cerebellar “black dots” are common in chronic hypertension but rare in CAA. Conversely,
peripheral (cortical, meningeal) “blooming black dots” on T2* are more common in CAA.
Strokes
“Stroke” is a generic term that describes a clinical event characterized by sudden onset of a neurologic deficit. However,
not all strokes are the same! Stroke syndromes have significant clinical and pathophysiological heterogeneity. Arterial
ischemia/infarction is by far the most common cause of stroke, accounting for 80% of all cases.
The remaining 20% of strokes are mostly hemorrhagic, divided among primary “spontaneous” (nontraumatic) intracranial
hemorrhage, nontraumatic subarachnoid hemorrhage, and venous occlusions.
As the clinical diagnosis of acute stroke is inaccurate in 15-20% of cases, imaging has become an essential component of
rapid stroke triage. When and how to image patients with suspected acute stroke varies from institution to institution.
Protocols are based on elapsed time since symptom onset, availability of emergent imaging with appropriate software
reconstructions, preferences of clinician (and radiologist), and availability of neurointervention.
There are four “must know” questions in stroke triage that must be answered quickly and accurately:
(1) Is intracranial hemorrhage or a stroke “mimic” present?
(2) Is a large vessel occluded?
(3) Is part of the brain irreversibly injured?
(4) Is there a clinically relevant “penumbra” of ischemic but potentially salvageable tissue?
The primary goal of “brain attack” protocols is to distinguish “bland” or ischemic stroke from intracranial hemorrhage and
to select/triage patients for possible reperfusion therapies. Most protocols begin with emergency NECT to answer the first
“must know” question: Is intracranial hemorrhage or a stroke mimic present? Once intracranial hemorrhage is excluded,
presence or absence of a major vessel occlusion can be determined noninvasively with CTA. The third and fourth
questions can be answered with either CT or MR perfusion.
P.II(1):3

Infections
The role of medical imaging in the emergent evaluation of a possible intracranial infection ideally should be supportive,

not primary. But in many health care facilities worldwide, a triage of acute CNS disease frequently uses brain imaging as
an initial noninvasive “screening procedure.”
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Diagnostic Imaging: Emergency
Meningitis is a clinical laboratory diagnosis, not a radiologic one. NECT scans in meningitis can be normal or show only
mild ventricular enlargement. Large ventricles with blurred margins on NECT scans indicate acute obstructive
hydrocephalus with accumulation of extracellular fluid in the deep periventricular white matter. Bone CT should be
carefully evaluated for sinusitis and otomastoiditis.
Encephalitis can be sporadic or epidemic. NECT scans in the most common nonepidemic encephalitis, i.e., herpes simplex
encephalitis, may be normal or show only hypodensity with mild mass effect in one or both temporal lobes. Patients with
suspected encephalitis are best evaluated with MR (including FLAIR and diffusion-weighted sequences).
Brain abscesses and empyemas are rare but potentially life-threatening CNS infections. Intraventricular rupture of a brain
abscess can be a catastrophic event. All these are serious disorders that are best evaluated with contrast-enhanced MR
(including FLAIR and diffusion-weighted sequences). Contrast-enhanced CT can also be performed if a screening NECT is
suggestive of either diagnosis.
Acute Toxic-Metabolic Derangements
A number of toxic and metabolic disorders present in the emergency department. In the absence of focal neurologic
deficit or altered mental status, emergent imaging is usually not indicated. There are some notable exceptions, e.g.,
pregnant patients with preeclampsia or eclampsia or hypertensive patients on chemotherapy. Posterior reversible
encephalopathy syndrome (PRES) is common in both scenarios. NECT scan is a good initial screening procedure. If it's
normal or equivocal, MR is more sensitive in subtle or atypical cases.
Seizures
Patients with first-time seizures and no neurologic deficit usually do not require emergent neuroimaging. A “screening”
NECT scan is relatively useless as subtle abnormalities are easily overlooked. Patients with recurrent, often drug-resistant
epilepsy are common ER visitors. Without trauma-associated brain injury, emergent neuroimaging is rarely indicated.
Complex febrile seizures are a common diagnosis in the pediatric emergency department. Recent studies have shown a
low likelihood of intracranial infections and abnormal neuroimaging findings.
Dizziness

Adults triaged to the ED with complaints of dizziness, vertigo, or imbalance pose a challenge to physicians. While dizziness
in the ED is generally benign, a substantial fraction of patients harbor serious neurologic disease such as stroke,
intracranial hemorrhage, transient ischemic attack, seizure, brain tumor, demyelinating disease, and CNS infection. Older
age, a chief complaint of imbalance, and focal neurologic abnormality are all independently associated with serious
neurologic diagnoses and may deserve emergent imaging. Imaging is usually negative in solated dizziness without other
abnormalities.
Head and Neck Emergencies
Patients may present to the emergency department with a wide variety of nontraumatic infectious, inflammatory, and
neoplastic conditions affecting the head and neck. Acute conditions that require emergent imaging are generally
restricted to trauma and suspected infections. Some can be potentially life threatening.
Oral cavity infections, tonsillitis and peritonsillar abscess, sialadenitis, parotiditis, thrombophlebitis, periorbital and orbital
cellulitis, infectious cervical lymphadenopathy, epiglottitis, invasive fungal sinusitis, and deep neck abscess all require
rapid diagnosis and treatment. CT is the first-line imaging modality in the emergency setting, and MR plays an important
secondary role.
Nontraumatic Emergencies Involving the Spine/Spinal Cord
While patients with back pain are common ER visitors, they generally do not require emergent imaging unless a focal
neurologic deficit is present.
True nontraumatic spinal emergencies are rare but represent a potential loss of function if not treated promptly and
properly. Patients with acute myelopathy, suspected infection, or cord ischemia as well as individuals with a known
malignancy and sudden onset of a neurologic deficit all require emergent imaging. MR is generally the procedure of
choice. A new imaging sequence—diffusion tensor imaging—can be very helpful in early detection of cord ischemia.
Selected References
1. Balestrini S et al: Emergency room access for recurring seizures: when and why. Eur J Neurol. Epub ahead of print, 2013
2. Boyle DA et al: Clinical factors associated with invasive testing and imaging in patients with complex febrile seizures.
Pediatr Emerg Care. 29(4):430-4, 2013
3. Wang X et al: Head CT for nontrauma patients in the emergency department: clinical predictors of abnormal findings.
Radiology. 266(3):783-90, 2013
4. Kelley BC et al: Spinal emergencies. J Neurosurg Sci. 56(2):113-29, 2012
5. Navi BB et al: Rate and predictors of serious neurologic causes of dizziness in the emergency department. Mayo Clin
Proc. 87(11):1080-8, 2012

6. Scheinfeld MH et al: Teeth: what radiologists should know. Radiographics. 32(7):1927-44, 2012
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Diagnostic Imaging: Emergency
7. Capps EF et al: Emergency imaging assessment of acute, nontraumatic conditions of the head and neck. Radiographics.
30(5):1335-52, 2010. Erratum in: Radiographics. 31(1):316, 2011
8. Crocker M et al: An extended role for CT in the emergency diagnosis of malignant spinal cord compression. Clin Radiol.
66(10):922-7, 2011
9. Jagoda A et al: The emergency department evaluation of the adult patient who presents with a first-time seizure. Emerg
Med Clin North Am. 29(1):41-9, 2011
10. Ludwig BJ et al: Diagnostic imaging in nontraumatic pediatric head and neck emergencies. Radiographics. 30(3):78199, 2010
11. Hardy JE et al: Computerized tomography of the brain for elderly patients presenting to the emergency department
with acute confusion. Emerg Med Australas. 20(5):420-4, 2008

Brain
Aneurysmal Subarachnoid Hemorrhage
> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Aneurysmal Subarachnoid
Hemorrhage
Aneurysmal Subarachnoid Hemorrhage
Perry P. Ng, MBBS (Hons), FRANZCR
Anne G. Osborn, MD, FACR
Key Facts
Terminology
SAH caused by ruptured aneurysm (aSAH)
Saccular (SA) > > dissecting aneurysm (DA)
Imaging
CT/CTA
Hyperdense sulci on NECT
Distribution varies with aneurysm location

Suprasellar cistern (IC-PCoA, ACoA aneurysms)
Sylvian fissure (MCA bifurcation)
Prepontine, CPA cisterns (PICA, BA bifurcation SA or vertebral DA)
CTA 90-95% positive if aneurysm ≥ 2 mm
MR/MRA
FLAIR hyperintense sulci, cisterns (nonspecific)
TOF MRA 85-95% sensitive for aneurysms ≥ 3 mm
DSA
Used if CTA negative
Endovascular treatment
Top Differential Diagnoses
Nonaneurysmal SAH
“Pseudo-SAH”
Reversible cerebral vasoconstriction syndrome (RCVS)
Clinical Issues
Sudden onset severe headache
“Thunderclap/worst headache of life”
50% mortality
Vasospasm 1-3 weeks post aSAH
20% rebleed within 1st 2 weeks
Treatment
Clipping vs. coil embolization (“coiling”)
Diagnostic Checklist
Diffuse low-density brain makes normal arteries look hyperdense, can mimic aSAH!

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Diagnostic Imaging: Emergency

(Left) Axial graphic through the midbrain depicts SAH in red throughout the basal cisterns. Given the diffuse distribution of
SAH without focal hematoma, statistically the most likely location of the ruptured aneurysm is the ACoA. (Right) Series of
axial NECT scans shows the typical appearance of aneurysmal SAH. Acute subarachnoid blood is seen as hyperdensity
in the basal cisterns, sylvian fissures, perimesencephalic cisterns, and interhemispheric fissure. Ruptured ACoA
aneurysm was found on CTA (not shown).

(Left) NECT scan shows diffuse basilar SAH
with more focal clot in the right anteromedial temporal lobe
and along
the right side of the suprasellar cistern
. (Right) 3D SSD of the right ICA angiogram in the same patient shows a large
trilobed IC-PCoA aneurysm
.
P.II(1):5

TERMINOLOGY
Abbreviations
Aneurysmal subarachnoid hemorrhage (aSAH)
Definitions
Extravasation of blood into subarachnoid space
Usually from ruptured saccular aneurysm
Less common: Intracranial dissecting aneurysm
IMAGING
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Diagnostic Imaging: Emergency
General Features
Best diagnostic clue
Hyperdense basal cisterns, sulci on NECT

Location
Suprasellar, basal, sylvian, interhemispheric cisterns
± intraventricular hemorrhage (IVH)
aSAH distribution depends on location of saccular aneurysm (SA)
aSAH highest near site of rupture
Anterior communicating artery (ACoA) aneurysm
→ anterior interhemispheric fissure
Middle cerebral artery (MCA) aneurysm → sylvian fissure
Basilar tip, superior cerebellar artery (SCA), posterior inferior cerebellar artery (PICA) SA, or
vertebral artery (VA) dissecting aneurysm (DA)
→ prepontine cistern, foramen magnum, 4th ventricle
“Culprit” aneurysm sometimes seen as filling defect within hyperdense aSAH
SAs typically located at bifurcation points along intradural ICA, circle of Willis (COW), MCA
90% located on anterior circulation: ACoA, posterior communicating artery (PCoA), MCA, carotid
terminus, carotid-ophthalmic, superior hypophyseal
10% on posterior circulation: Basilar tip, PICA, anterior inferior cerebellar artery (AICA), SCA
DAs: Intradural V4 VA segment most common
Blood-blister aneurysm (BBA)
Dorsal supraclinoid ICA
Rarely MCA, basilar artery
CT Findings
NECT
95% positive in 1st 24 hours, < 50% by 1 week
“Effaced” sylvian fissure if subacute, filled with isodense SAH
Hydrocephalus common, may occur early
± intraparenchymal hemorrhage at site of ruptured aneurysm
CTA
90-95% positive if aneurysm ≥ 2 mm
MR Findings
T1WI

Acute aSAH is isointense to CSF
CSF may appear mildly hyperintense (“dirty”)
T2WI
Difficult to see on T2WI (hyperintense), GRE
FLAIR
Hyperintense
More sensitive than CT but less specific
DWI
May see foci of restricted diffusion if vasospasm
MRA
TOF MRA 85-95% sensitive for aneurysms ≥ 3 mm
Angiographic Findings
Conventional “4-vessel angiogram” = gold standard
Must image
Both ICA circulations
Both VAs or dominant VA + reflux to contralateral PICA
SA
Saccular outpouching at arterial branch point
Look for Murphy teat = site of rupture
Look for additional aneurysms (20% multiple)
If > 1 aneurysm, then biggest, most irregular ± adjacent vasospasm is likely source of bleed
DA
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Diagnostic Imaging: Emergency
Irregular ± dilated or stenotic V4 segment of VA
BBA
Smooth/irregular bleb/dome-shaped outpouching
Not associated with major vessel branch point

Most common along supraclinoid ICA
DSA negative in 15% of aSAH; repeat positive < 5%
Evaluate ECAs (to exclude dural AV fistula [dAVF])
SA may not be seen on initial DSA if optimal projection not obtained, spontaneous partial or
complete aneurysm thrombosis, &/or presence of vasospasm
Consider repeating DSA in 5-7 days
Imaging Recommendations
Best imaging tool
NECT + multiplanar CTA
Protocol advice
Proceed to DSA if NECT consistent with aSAH but CTA negative
Consider MR if DSA + CTA negative
DIFFERENTIAL DIAGNOSIS
Nonaneurysmal SAH
Perimesencephalic SAH
Small SAH, localized to interpeduncular cistern
Presumed venous etiology with low recurrence rate
Traumatic subarachnoid hemorrhage
Adjacent to contusions, subdural hematomas
Rarely from intracranial dissection or rupture of traumatic pseudoaneurysm
Subarachnoid hemorrhage, NOS
Vascular malformation: Arteriovenous malformation (AVM), cavernous hemangioma
Reversible Cerebral Vasoconstriction Syndrome (RCVS)
Clinical: “Thunderclap” headache
SAH typically in cortical sulci vs. basal cisterns with aSAH
“Pseudo-SAH”
Hypodense brain: Severe cerebral edema
Hyperdense CSF: Intrathecal contrast; meningitis
P.II(1):6

PATHOLOGY
General Features
Etiology
Saccular aneurysms
Berry aneurysms: Congenital deficiency of internal elastic lamina and tunica media at arterial branch
points → focal vessel wall weakness
↑ risk: Familial intracranial aneurysms (5% of cases), adult polycystic kidney disease, aortic
coarctation
May be related to high-flow arteriopathy along feeding vessel of AVM or, less commonly, dAVF
↑ aneurysm rupture risk if female, smoker, HTN
Fusiform aneurysms
Dissection from trauma, hypertension, ASVD
Underlying arteriopathy including fibromuscular dysplasia (FMD), Marfan, Ehlers-Danlos, infection
Mycotic
Blood-blister aneurysm: All layers absent (contained in fibrous cap)
Associated abnormalities
Vasospasm
Caused by blood breakdown products, apolipoprotein E genotype, endothelin-1 release from CSF
leukocytes
70% develop angiographic evidence of vasospasm
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Diagnostic Imaging: Emergency
30% have clinically apparent vasospasm
Starts ˜ day 3-4 post SAH; peaks ˜ 7-9 days, lasts ˜ 12-16 days
Cerebral salt-wasting syndrome
Excessive renal Na+ excretion → hyponatremia, hypovolemia
Terson syndrome
Intraocular (retinal, vitreous) hemorrhage associated with SAH secondary to rapid ↑ intracranial

pressure
Staging, Grading, & Classification
Clinical grading: Hunt and Hess (H&H) grade 0-5
0: No SAH (unruptured aneurysm)
1: No symptoms, minimal headache, slight nuchal rigidity
2: Moderate to severe headache, nuchal rigidity
No neurologic deficit except CN palsy
3: Drowsy, minimal neurologic deficit
4: Stuporous, moderate/severe hemiparesis
5: Coma, decerebrate rigidity, moribund appearance
WFNS clinical grading system: Based on GCS and presence/absence of major focal neurological deficit
Fisher CT grading
1: No SAH visible
2: Diffuse, thin layer (< 1 mm)
3: Localized clot or thick layer (> 1 mm)
4: Intraventricular blood
Gross Pathologic & Surgical Features
Blood in basal cisterns, sulci, and ventricles
CLINICAL ISSUES
Presentation
Most common signs/symptoms
Sudden “thunderclap/worst headache of life”
10% preceded by “sentinel hemorrhage” = self-limiting SAH + headache in preceding days/weeks
Demographics
Age
Peak = 40-60 years
Gender
M:F = 1:2
Epidemiology
Aneurysms cause 85% of spontaneous SAHs

Incidence ˜ 9.9 per 100,000 population
Natural History & Prognosis
50% mortality; 20% rebleed within 1st 2 weeks
Clinical outcome inversely proportional to initial H&H or WFNS grade
Vasospasm + ischemia → delayed morbidity, mortality
Severity correlates with amount of SAH (Fisher CT grade); inverse correlation with patient age
90% hydrocephalus at presentation
˜ 10% require permanent CSF diversion
Treatment
Ruptured aneurysm
Microneurosurgical clipping
Proven effective over decades but invasive, higher morbidity/mortality compared with coiling
1 study: Death or dependence at 1 year = 23.7% with coiling vs. 30.7% with clipping
Coil embolization (“coiling”), if anatomy favorable
Platinum coils ± bioactive coating to reduce recurrence rate
Aneurysm recurrence > surgical clipping but low risk of recurrent SAH
Vasospasm
Ca++ antagonists, “triple-H” therapy (hypervolemia, hemodilution, hypertension)
Endovascular: Intraarterial Ca++ antagonist (“chemical angioplasty”), balloon angioplasty
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Diagnostic Imaging: Emergency
Hydrocephalus
Temporary or permanent CSF diversion
Cerebral salt-wasting syndrome
Na+ tablets or IV hypertonic saline
DIAGNOSTIC CHECKLIST
Consider
Nonaneurysmal SAH if characteristic blood distribution (e.g., perimesencephalic SAH, RCVS)

Look for multiple aneurysms and decide which most likely bled
Image Interpretation Pearls
Isodense SAH: Anterior 3rd ventricle and temporal horns are only CSF density structures at base of brain; absence of
sylvian fissure(s)
SELECTED REFERENCES
1. Farzad A et al: Emergency diagnosis of subarachnoid hemorrhage: an evidence-based debate. J Emerg Med. 44(5):104553, 2013
2. Froehler MT: Endovascular treatment of ruptured intracranial aneurysms. Curr Neurol Neurosci Rep. 13(2):326, 2013
P.II(1):7

Image Gallery

(Left) NECT scan in a patient with sudden onset of the “worst headache of my life” shows aSAH in the suprasellar cistern
and sylvian fissures
. A “filling defect”
is present within the blood in the anteroinferior aspect of the
interhemispheric fissure. (Right) CTA in the same case shows a 6 mm saccular aneurysm
arising from the anterior
communicating artery.

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Diagnostic Imaging: Emergency

(Left) Sagittal T1WI illustrates typical findings of acute aneurysmal SAH. Note “dirty” CSF
that appears isointense with
adjacent brain. The normal basilar artery “flow void”
is surrounded by the SAH. (Right) Axial T1WI in the same case
shows a nice contrast between the isointense (with brain) “dirty” CSF
and the more normal-appearing hypointense

(“dark”) CSF in the cistern
and temporal horns
.

(Left) T2WI in the same patient shows that the hyperintense SAH is difficult to distinguish from the normal “bright” CSF
. The SAH
is very slightly less hyperintense than the adjacent CSF. (Right) Normal CSF suppresses on FLAIR. FLAIR
scan in the same case shows CSF in the suprasellar cistern
is abnormally hyperintense. Sulcal-cisternal hyperintensity
is also seen in the left perimesencephalic and superior cerebellar cisterns as well as the parietooccipital subarachnoid
spaces
.

Nonaneurysmal Perimesencephalic SAH
> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Nonaneurysmal
Perimesencephalic SAH
Nonaneurysmal Perimesencephalic SAH
Gary M. Nesbit, MD
Anne G. Osborn, MD, FACR
Key Facts
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Diagnostic Imaging: Emergency
Terminology
Clinically benign SAH confined to perimesencephalic, prepontine cisterns
No source demonstrated at angiography
Imaging
CT: Hyperdense prepontine, perimesencephalic CSF
T1: Iso- to hyperintense

T2 variable (iso- to hyper-) intensity compared to CSF
FLAIR: Hyperintense prepontine, perimesencephalic CSF
May be mimicked by CSF pulsation artifact or in ventilated patients with > 50% O2 concentration
Normal DSA required to exclude aneurysm or other cause and confirm diagnosis
MR/MRA may confirm alternative diagnosis and negate need for repeat DSA
Pathology
Most likely cause: Ruptured perimesencephalic/prepontine vein
Other nonaneurysmal causes: Intracranial dissection, vasculitis, trauma, dural AV fistula, spinal vascular
malformation; have less benign course
Vertebrobasilar aneurysms, dissection may have pnSAH pattern
Clinical Issues
Benign course: Rebleed rare (< 1%); no vasospasm
Headache (usually Hunt/Hess grade 1 or 2), often intra-/post coitus
More extensive pnSAH may develop hydrocephalus or intraventricular blood

(Left) Axial graphic shows a classic pnSAH. Hemorrhage is confined to the interpeduncular fossa and ambient
(perimesencephalic) cisterns . The source is usually venous in pnSAHs, unlike in aneurysmal SAHs. (Right) NECT scans in
a patient with pnSAH show blood in the prepontine, perimesencephalic/ambient cisterns
but in the not anterior
suprasellar cistern or sylvian fissures. DSA was negative.

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Diagnostic Imaging: Emergency

(Left) NECT scan in a 39-year-old woman in the ER complaining of the “worst headache of my life” shows isolated
subarachnoid hemorrhage in the interpeduncular fossa
. There is no blood in the suprasellar cistern
or sylvian

fissures
. The ventricles are normal with no evidence for hydrocephalus. (Right) CTA with MIP axial projection in the
same patient shows no evidence of aneurysm.
P.II(1):9

TERMINOLOGY
Abbreviations
Perimesencephalic nonaneurysmal subarachnoid hemorrhage (pnSAH)
Synonyms
Benign perimesencephalic SAH
Definitions
Clinically benign SAH confined to perimesencephalic, prepontine cisterns
No source demonstrated at angiography
IMAGING
General Features
Best diagnostic clue
Hyperdense prepontine, perimesencephalic CSF
Location
Subarachnoid cisterns around midbrain and anterior to pons
CT Findings
NECT
High attenuation anterior to pons and around midbrain
No supratentorial extension
MR Findings
T1WI
Iso- to hyperintense CSF around midbrain
Focal clot around basilar artery
T2WI
Variable; iso- to hypointense blood in CSF
FLAIR

Hyperintense CSF is more extensive than on T1/T2
Mimicked by CSF pulsation artifact
T2* GRE
Hypointense thrombus in CSF
Angiographic Findings
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Diagnostic Imaging: Emergency
CTA/MRA/DSA
No source of hemorrhage identified
Normal DSA required to confirm diagnosis
Imaging Recommendations
Best imaging tool
NECT best screening for pnSAH
DSA to exclude aneurysm
MR/MRA may confirm SAH or cause; may negate need for repeat DSA
Protocol advice
NECT with CTA
MR/MRA may help confirm diagnosis
Consider cervical MR to exclude rare spinal vascular source
DIFFERENTIAL DIAGNOSIS
Aneurysmal SAH
More extensive hemorrhage
Vertebrobasilar aneurysms may have pnSAH pattern
Traumatic SAH
Perisylvian, convexity more common than perimesencephalic pattern
Artifact: FLAIR
Incomplete CSF suppression
> 50% O2 concentration

PATHOLOGY
General Features
Etiology
Most likely cause: Ruptured perimesencephalic/prepontine vein
Other nonaneurysmal causes have less benign course
Intracranial dissection, vasculitis, trauma, dural AV fistula, spinal cord vascular malformation
Vertebrobasilar aneurysms, dissection may have pnSAH pattern
Gross Pathologic & Surgical Features
Clotted blood in perimesencephalic cisterns
Similar to aneurysmal SAH
CLINICAL ISSUES
Presentation
Most common signs/symptoms
Headache (usually Hunt/Hess grade 1 or 2)
Often post coitus
Demographics
Age: 40-60 years
Gender: M = F
Epidemiology
Majority of angiogram-negative SAH
Natural History & Prognosis
Benign course: Rebleed rare (< 1%); no vasospasm
More extensive pnSAH may develop hydrocephalus or intraventricular blood
Treatment
Monitoring and treatment of rare secondary hydrocephalus, vasospasm
DIAGNOSTIC CHECKLIST
Consider
Occult trauma, vertebral dissection, vasculitis, dural AV fistula, or spinal vascular malformation
Image Interpretation Pearls
DSA needed to exclude aneurysm, other vascular cause

Perimesencephalic thrombus and focal clot around basilar artery on MR
SELECTED REFERENCES
1. Kim YW et al: Nonaneurysmal subarachnoid hemorrhage: an update. Curr Atheroscler Rep. 14(4):328-34, 2012

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Diagnostic Imaging: Emergency
2. Kong Y et al: Perimesencephalic subarachnoid hemorrhage: risk factors, clinical presentations, and outcome. Acta
Neurochir Suppl. 110(Pt 1):197-201, 2011

Saccular Aneurysm
> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Saccular Aneurysm
Saccular Aneurysm
Perry P. Ng, MBBS (Hons), FRANZCR
Anne G. Osborn, MD, FACR
Key Facts
Terminology
Intracranial saccular aneurysm (SA)
Outpouching affecting only part of arterial circumference
Lacks internal elastic lamina ± tunica media
Imaging
Round/lobulated arterial outpouching
Usually arises from bifurcations of circle of Willis (COW), supraclinoid ICA, MCA, cerebellar arteries
90% occur in anterior circulation
10% posterior circulation: Basilar tip, cerebellar arteries (PICA most common)
Rare (< 1%): Trigeminal artery, vertebrobasilar junction fenestration
Ruptured SAs result in SAH
May have mural Ca++
Sensitivity of multislice CTA > 95% for SA > 2 mm

3D TOF: > 90% sensitive for aneurysms ≥ 3 mm
Top Differential Diagnoses
Vessel loop
Vessel infundibulum
Fusiform aneurysm
Flow void MR mimic (e.g., aerated anterior clinoid)
Clinical Issues
Vast majority of unruptured SAs are asymptomatic
2-6% incidental finding at autopsy, imaging
80-90% of nontraumatic SAH caused by ruptured SA
Treatment
Endovascular coiling vs. surgical clipping
22.6% relative, 6.9% absolute risk ↓ for coiling vs. surgery for ruptured aneurysms
↓ morbidity, mortality, and hospital costs; quicker recovery for unruptured aneurysms

(Left) Most common sites for SAs are ACoA

and IC-PC junction
764

. MCA bifurcation

and basilar tip

are other


Diagnostic Imaging: Emergency
frequent sites. (Right) Graphic illustrates rupture of an ACoA aneurysm
with active extravasation from a superiorly

directed bleb (Murphy teat). An additional posterior communicating artery SA
and tiny bleb at the left MCA bifurcation
are seen. Patients with SAs have a 20% chance of having > 1 aneurysm.

(Left) Most intracranial SAs present with subarachnoid hemorrhage. In this case, SAH is present in the basilar cisterns
.
A focal temporal lobe hematoma
with a rounded “filling defect”
is present. (Right) CTA in the same case shows a
right MCA trifurcation saccular aneurysm
.
P.II(1):11

TERMINOLOGY
Abbreviations
Intracranial saccular aneurysm (SA)
Synonyms
Berry aneurysm, true aneurysm
Definitions
Arterial outpouching affecting only part of arterial circumference
Lacks internal elastic lamina ± tunica media
IMAGING
General Features
Best diagnostic clue
Round/lobulated arterial outpouching
Usually arises from bifurcations of circle of Willis (COW), supraclinoid ICA, MCA, cerebellar arteries
Location
90% occur in anterior circulation
ACoA, PCoA, MCA bifurcation, carotid terminus most common sites
Other: Paraclinoid ICA, superior hypophyseal, anterior choroidal artery (AChA)

10% posterior circulation: Basilar tip, cerebellar arteries (PICA most common)
Rare (< 1%): Trigeminal artery, vertebrobasilar junction fenestration
Vessel bifurcation > side wall aneurysm (e.g., blood blister-like aneurysm)
Size
Small (< 3 mm) to giant (> 2.5 cm)
Morphology
Round, ovoid daughter lobe(s)
Narrow or wide necked
Branch vessel may be incorporated into aneurysm neck (can preclude coil embolization)
CT Findings
NECT
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Diagnostic Imaging: Emergency
Ruptured SAs result in subarachnoid hemorrhage (SAH)
Pattern of SAH may help localize SA location
If SA contains thrombus → hyperdense to brain
May have mural Ca++
CECT
Lumen of patent SA enhances uniformly
Completely thrombosed SA may have rim enhancement
CTA
Sensitivity of multislice CTA > 95% for SA > 2 mm
Look for > 1 aneurysm, as SA is multiple in 20% of patients
Look for associated SAH vasospasm if ruptured SA
Alternative to DSA as first imaging technique in SAH
MR Findings
T1WI
Patent aneurysm (signal varies)

50% have flow void
50% iso-/heterogeneous signal (slow/turbulent flow, saturation effects, phase dispersion)
Partially/completely thrombosed aneurysm
Signal depends on age of thrombus
Common: Mixed signal, laminated thrombus
Hypointense + “blooming” on susceptibility sequences (GRE, SWI)
T2WI
Typically hypointense (flow void)
May be laminated with very hypointense rim
FLAIR
Acute SAH: High signal in sulci, cisterns
DWI
May see restricted diffusion secondary to ischemia from SAH vasospasm
Thromboembolic events from intraaneurysmal thrombus (rare)
T1WI C+
Slow flow in patent lumen may enhance
Increased phase artifact in patent SAs
MRA
3D TOF: > 90% sensitive for aneurysms ≥ 3 mm
Short T1 substances, such as subacute hemorrhage, may simulate flow on TOF MRA
Angiographic Findings
Conventional DSA
Technique
Bilateral carotid + dominant vertebral artery injections with reflux to contralateral PICA or “4 vessel”
cerebral DSA required
Cross-compression of contralateral carotid may be needed for evaluation of ACoA
Rotational DSA with 3D surface-shaded display (SSD) reconstructions may be helpful but prone to
artifact depending on window settings
Rare: Contrast extravasation with active SAH
Look for Murphy teat (bleb at site of recent rupture) vs. daughter lobe (smaller outpouching from aneurysm

fundus, likely indicating focal wall weakness, ↑ future rupture risk)
Imaging Recommendations
Best imaging tool
NECT + CTA for work-up of SAH
CTA or MRA for screening of high-risk groups
Protocol advice
Dual energy direct bone removal CT angiography for evaluation of skull base/paraclinoid SA
3D SSD reconstructions helpful to visualize ACoA and MCA bifurcation
DIFFERENTIAL DIAGNOSIS
Vessel Loop
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Diagnostic Imaging: Emergency
Use multiple projections
Vessel Infundibulum
< 3 mm, conical, vessel arises directly from apex
Commonly at posterior communicating artery (PCoA) and anterior choroidal artery (AChA) origins
Fusiform Aneurysm
Sausage-shaped morphology with separate inflow, outflow pathways
Long segment, usually located distal to COW
Can be secondary to ASVD
Often pseudoaneurysm etiology
P.II(1):12

Trauma, mycotic, vasculitic, connective tissue disease
Flow Void (MR Mimic)
Aerated anterior clinoid or supraorbital cell
PATHOLOGY
General Features

Etiology
SA development and rupture risk reflect complex combination of inherited susceptibility + acquired
mechanically mediated vessel wall stresses
Abnormal vascular hemodynamics → ↑ wall stress
Flow-related “bioengineering fatigue” in vessel wall more likely with asymmetric COW → ↑
development of SA at site of anomaly
e.g., aplastic A1 segment, persistent trigeminal artery, vertebrobasilar fenestration
Genetics
Familial intracranial aneurysms (FIAs)
No known heritable connective tissue disorder
Occur in “clusters” (1st-order relatives)
Younger patients, no female predominance compared to sporadic SAs
Consider screening with CTA or MRA
Associated abnormalities
↑ SA incidence in patients with
Fibromuscular dysplasia (FMD): Autosomal dominant, sporadic
Bicuspid aortic valve
Autosomal dominant polycystic kidney disease (10% have SA)
Intracranial AVM: Feeding pedicle (“flow-related”) aneurysms in 30%
May regress after treatment of AVM
Gross Pathologic & Surgical Features
Round/lobulated sac, thin or thick wall, ± SAH
Microscopic Features
Disrupted/absent internal elastic lamina
Muscle layer absent
May have “teat” of fragile adventitia
CLINICAL ISSUES
Presentation
Most common signs/symptoms
Vast majority of unruptured SA are asymptomatic

Cranial neuropathy uncommon (e.g., pupil-involving CN3 palsy from PCoA aneurysm)
TIA/stroke from thromboembolic events secondary to intraaneurysmal thrombus (rare)
80-90% of nontraumatic SAH caused by ruptured SA
Headache (typical = “thunderclap”)
Clinical profile
2 common scenarios
Middle-aged patient with “worst headache of my life” from ruptured SA → SAH
Incidental finding on imaging performed for unrelated symptoms in patient of any age
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Diagnostic Imaging: Emergency
Demographics
Age
↑ incidence of SA with age; rare in children
Gender
M < F (especially with multiple aneurysms)
Epidemiology
2-6% incidental finding of unruptured SA at autopsy
Annual risk of de novo aneurysm formation = 0.8% in patients with previous SA
Natural History & Prognosis
Rupture risk
Size: Low risk of SA rupture if < 7 mm
Growth, rupture risk for unruptured aneurysms
Growth rate = 3.9% per year
1.8% per year rupture risk
˜ 20% of ruptured unsecured SA rebleed within 2 weeks, 50% in 6 months
Shape: Daughter lobe likely ↑ risk of future SAH; Murphy teat = site of recent rupture and possible rebleed if
untreated
↑ in females with history of HTN, smoking

Treatment
Endovascular coiling
Ruptured SA: 22.6% relative, 6.9% absolute risk ↓ for coiling vs. surgery (1 study)
Unruptured SA: Coiling vs. clipping
↓ morbidity, mortality, and hospital costs; shorter hospital stay; quicker recovery
Surgical clipping
Lower SA recurrence risk compared with coiling, although rebleeding risk is low with either Rx
May have advantage in MCA and other SA where branch vessel arising from SA must be preserved
DIAGNOSTIC CHECKLIST
Consider
Blood blister-like aneurysm if negative CTA in patient with SAH → perform DSA
Perimesencephalic bleed in patient with blood localized to interpeduncular cistern
Image Interpretation Pearls
Diffuse SAH without focal hematoma → ACoA is most likely site of ruptured SA
Absence of sylvian fissures may be clue to subacute (isodense) SAH
SELECTED REFERENCES
1. Matsumoto K et al: Incidence of growth and rupture of unruptured intracranial aneurysms followed by serial MRA. Acta
Neurochir (Wien). 155(2):211-6, 2013
2. Rabinstein AA: Subarachnoid hemorrhage. Neurology. 80(5):e56-9, 2013
3. Vasan R et al: Pediatric intracranial aneurysms: current national trends in patient management and treatment. Childs
Nerv Syst. 29(3):451-6, 2013
4. Wang H et al: 320-detector row CT angiography for detection and evaluation of intracranial aneurysms: comparison
with conventional digital subtraction angiography. Clin Radiol. 68(1):e15-20, 2013
5. Cianfoni A et al: Clinical presentation of cerebral aneurysms. Eur J Radiol. Epub ahead of print, 2012
P.II(1):13

Image Gallery

768

Diagnostic Imaging: Emergency

(Left) Patent saccular aneurysms are seen as rounded hypointense “flow voids” on MR. This saccular aneurysm at the
distal ICA bifurcation
was found incidentally on the T2WI of this elderly patient. (Right) Thrombosed SAs can appear
very hyperdense. This patient presented in the ER with sudden onset of right hemiparesis. NECT scan, obtained as the
initial study in the standard stroke protocol, shows an ovoid hyperdensity
with what appears to be thrombus in the
left proximal MCA
.

(Left) Source image from the CTA in the same patient shows abrupt “cut-off” of the left MCA
and non-filling of a large,
completely thrombosed saccular aneurysm
. (Right) CT perfusion study in the same case shows markedly decreased
cerebral blood flow in the left MCA distribution
. The basal ganglia (supplied by lenticulostriate branches from the
unoccluded proximal MCA) are spared. Cerebral infarction can be caused by distal migration of clot from a thrombosed
SA.

769


Diagnostic Imaging: Emergency

(Left) Some aneurysms exhibit mural calcification. NECT scan shows an incidentally discovered SA, seen here as a welldemarcated rounded hyperdensity
with a peripheral rim of calcification
. (Right) CTA was subsequently performed
in the same case. Coronal MIP shows a patent saccular aneurysm

at the terminal bifurcation of the left ICA.

Spontaneous Intracranial Hemorrhage
> Table of Contents > Part II - Nontrauma > Section 1 - Central Nervous System > Brain > Spontaneous Intracranial
Hemorrhage
Spontaneous Intracranial Hemorrhage
Laurie A. Loevner, MD
Anne G. Osborn, MD, FACR
Key Facts
Terminology
Primary intraparenchymal hemorrhage
Acute nontraumatic intracranial hemorrhage (ICH)
Imaging
Tiny “microbleeds” to massive lobar hematoma
Peripheral edema
Hematoma location vs. common causes of pICH
HTN: Basal ganglia, thalamus, pons, cerebellum
Amyloid angiopathy: Microbleeds, lobar hemorrhages
Arteriovenous malformation: Any location
Cavernous malformation: Any location
Venous sinus thrombosis: Subcortical white matter
Neoplasm: Any location
May have fluid-fluid level: Coagulopathy, brisk bleeding, underlying cystic mass
Recommended imaging protocol
Start with NECT
If HTN with striatocapsular hematoma, no further imaging necessary
If unclear history, CTA
Atypical hematoma: MR (T2*, DWI, T1 C+)
Follow-up: Repeat MR if etiology unclear ± DSA if initial MRA/CTA negative
Pathology

Child < 15? Think AVM!
Young adult? Vascular malformation, drug abuse, venous thrombosis, vasculitis
Patient > 45 years old? HTN, amyloid, venous infarct, neoplasm (primary or metastatic), coagulopathy
Clinical Issues
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Diagnostic Imaging: Emergency
sICH causes 15-20% of acute strokes
Control of ICP, hydrocephalus critical
Surgical evacuation when clinically indicated

(Left) A 15-year-old male presented in the ER with sudden-onset severe headache and right-sided weakness. NECT scan
shows an acute temporal lobe hematoma
. (Right) Lateral view of the left internal carotid angiogram in the same case
shows a large left temporal lobe mass effect with a tightly packed “tangle” of vessels
and an “early draining vein”
consistent with hemorrhagic, partially-thrombosed AVM.

(Left) A 23-year-old male with a cocaine overdose presented in the ER with severe headache and left-sided weakness.
Blood pressure was 220/120 on admission. NECT scan shows a classic hypertensive right putamen-external capsule
hemorrhage
. (Right) A 34-year-old male with headache and right-sided weakness was sent from the ER for emergent
imaging. NECT scan shows a right parietal hematoma
. The superior sagittal sinus
appears more dense than
normal. Thrombosed SSS, cortical vein caused this sICH.
P.II(1):15

TERMINOLOGY

Synonyms
Primary intraparenchymal hemorrhage (pICH), stroke
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Diagnostic Imaging: Emergency
Definitions
Spontaneous (nontraumatic) intracranial hemorrhage (sICH)
Etiology often initially unknown
IMAGING
General Features
Best diagnostic clue
Acute nontraumatic intracerebral hematoma
Location
Varies with etiology
Hypertension (HTN): Deep gray matter (basal ganglia, thalamus), pons, cerebellar hemisphere
Amyloid angiopathy: Lobar
Arteriovenous malformation (AVM): Any location
Cavernous malformation: Any location, common in brainstem
Venous sinus thrombosis: Subcortical white matter adjacent to occluded sinus
Neoplasm: Any location
Size
Subcentimeter “microbleeds” to massive hemorrhage
Morphology
Typically round or oval; often irregular when large
Patterns with HTN and amyloid angiopathy
Acute parenchymal hematoma
Multiple subacute/chronic “microbleeds” in deep gray matter (HTN > amyloid) &/or subcortical
white matter (amyloid > HTN)
Microbleeds often seen only on GRE MR

CT Findings
NECT
Acute hyperdense round/elliptical mass
May be mixed iso-/hyperdense
May have fluid-fluid level
Coagulopathy
Brisk bleeding
Bleed into cystic mass
Peripheral low density (edema)
Deep (ganglionic) ICH may rupture into lateral ventricle
CTA
Look for “spot sign” (contrast extravasation in hematoma)
Predicts subsequent hematoma expansion
Associated with increased morbidity/mortality
Look for dural sinus venous thrombosis
MR Findings
T1WI
Hyperacute (< 6 hours)
Isointense center (oxygenated Hgb)
Isointense periphery (deoxygenated Hgb, clot-tissue interface)
Hypointense rim (vasogenic edema)
T2WI
Hyperacute (< 6 hours)
Iso-/hyperintense, heterogeneous center
Hypointense periphery
Hyperintense rim of edema
T2* GRE
Hypointense
Multifocal hypointense lesions (“black dots”)
Basal ganglionic suggests HTN

Subcortical WM suggests amyloid angiopathy
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Diagnostic Imaging: Emergency
DWI
T2 “shine through” common
T1WI C+
May enhance if underlying neoplasm, vascular malformation
MRA
Often normal
MRV
Look for dural sinus thrombosis
Angiographic Findings
DSA, often negative
Look for dural sinus occlusion, “stagnating vessels” (thrombosed AVM)
Imaging Recommendations
Best imaging tool
Start with NECT
If patient with HTN and striatocapsular hematoma, no further imaging necessary
If unclear history, add CTA
Standard MR (include T2*, DWI)
If no clear cause of hemorrhage, or atypical appearance on CT
T1WI C+ to assess for underlying tumor
If standard study suggests vascular etiology → MRA
Consider DSA if initial MRA/CTA negative
Follow-up: Repeat MR if etiology remains unclear
Protocol advice
Add CTA to NECT if unclear history
If atypical/unexplained hematoma, consider adding MR (with T2*, DWI, T1WI C+)

DIFFERENTIAL DIAGNOSIS
Hypertensive Intracranial Hemorrhage
Patients usually older
Basal ganglionic hematoma most common
Cerebral Amyloid Angiopathy
Older patients (70 years old, normotensive)
Usually lobar
Microbleeds (“black dots”) on T2*
Underlying Neoplasm
Causes 2-15% of nontraumatic ICHs
Primary (glioblastoma multiforme) or metastasis
May show enhancement
Vascular Malformation
AVM, cavernous malformation most common
ICH rate in AVMs of basal ganglia or thalamus (9.8% per year) much higher than AVMs in other locations
Cortical Venous Thrombosis
Adjacent dural sinus often thrombosed
Anticoagulation
“Growing” hematoma, fluid-fluid levels common
P.II(1):16

Check history
Drug Abuse
May have hypertensive striatocapsular hemorrhage
Uncommon = pseudoaneurysm rupture into cerebrum
Vasculitis
Less common cause of spontaneous ICH
Patients usually younger
Dural AVF (With Cortical Venous Drainage)
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Diagnostic Imaging: Emergency
Dilated venous “flow voids”
Ruptured Pseudoaneurysm
Mycotic (endocarditis)
Traumatic
Vasculopathy
PATHOLOGY
General Features
Etiology
Child < 15? Think AVM!
Young adult? Vascular malformation, drug abuse, venous thrombosis, vasculitis
Patient > 45 years old? HTN, amyloid, venous infarct, neoplasm (primary or metastatic), coagulopathy
Genetics
MMP-9, cytokine gene expression ↑ after acute spontaneous ICH
Staging, Grading, & Classification
Clinical “ICH score” correlates with 30-day mortality
Admission GCS
> 80 years old, ICH volume
Infratentorial
Presence of intraventricular hemorrhage
Gross Pathologic & Surgical Features
Findings range from petechial “microbleeds” to gross parenchymal hematoma
Microscopic Features
Coexisting microangiopathy common in amyloid, HTN
CLINICAL ISSUES
Presentation
Most common signs/symptoms
90% of patients with recurrent pICH are hypertensive

Large ICHs present with sensorimotor deficits, impaired consciousness
Demographics
Age
Perinatal through elderly
Epidemiology
Causes 15-20% of acute strokes
Natural History & Prognosis
Prognosis related to location, size of ICH
Hematoma enlargement common in 1st 24-48 hours
Risk factors: EtOH, low fibrinogen, coagulopathy, irregularly shaped hematoma
Edema associated with poor outcome
Mortality: 30-55% in 1st month
30% rebleed within 1 year
Most survivors have significant deficits
Treatment
Control of ICP, hydrocephalus
Surgical evacuation when clinically indicated
DIAGNOSTIC CHECKLIST
Consider
Underlying etiology for hemorrhage (AVM, amyloid, neoplasm, drug use, etc.)
Image Interpretation Pearls
Unexplained ICH → search for microbleeds on T2* MR
Fluid-fluid level, iso-/mildly hyperdense clot may indicate coagulopathy
SELECTED REFERENCES
1. Freeman WD et al: Intracranial hemorrhage: diagnosis and management. Neurol Clin. 30(1):211-40, ix, 2012
2. Khosravani H et al: Emergency noninvasive angiography for acute intracerebral hemorrhage. AJNR Am J Neuroradiol.
Epub ahead of print, 2012
3. Thanvi BR et al: Advances in spontaneous intracerebral haemorrhage. Int J Clin Pract. 66(6):556-64, 2012
774

Diagnostic Imaging: Emergency
4. Fischbein NJ et al: Nontraumatic intracranial hemorrhage. Neuroimaging Clin N Am. 20(4):469-92, 2010
5. Hanley DF: Intraventricular hemorrhage: severity factor and treatment target in spontaneous intracerebral hemorrhage.
Stroke. 40(4):1533-8, 2009
6. Jeffree RL et al: Warfarin related intracranial haemorrhage: a case-controlled study of anticoagulation monitoring prior
to spontaneous subdural or intracerebral haemorrhage. J Clin Neurosci. 16(7):882-5, 2009
7. Kumar R et al: Spontaneous intracranial hemorrhage in children. Pediatr Neurosurg. 45(1):37-45, 2009
8. Tejero MA et al: [Multiple spontaneous cerebral haemorrhages. Description of a series and review of the literature.] Rev
Neurol. 48(7):346-8, 2009
9. Walsh M et al: Developmental venous anomaly with symptomatic thrombosis of the draining vein. J Neurosurg.
109(6):1119-22, 2008
10. Harden SP et al: Cranial CT of the unconscious adult patient. Clin Radiol. 62(5):404-15, 2007
11. Chao CP et al: Cerebral amyloid angiopathy: CT and MR imaging findings. Radiographics. 26(5):1517-31, 2006
12. Finelli PF: A diagnostic approach to multiple simultaneous intracerebral hemorrhages. Neurocrit Care. 4(3):267-71,
2006
13. Leach JL et al: Imaging of cerebral venous thrombosis: current techniques, spectrum of findings, and diagnostic pitfalls.
Radiographics. 26 Suppl 1:S19-41; discussion S42-3, 2006
14. Thanvi B et al: Sporadic cerebral amyloid angiopathy—an important cause of cerebral haemorrhage in older people.
Age Ageing. 35(6):565-71, 2006
15. Chalela JA et al: Multiple cerebral microbleeds: MRI marker of a diffuse hemorrhage-prone state. J Neuroimaging.
14(1):54-7, 2004
16. Skidmore CT et al: Spontaneous intracerebral hemorrhage: epidemiology, pathophysiology, and medical management.
Neurosurg Clin N Am. 13(3):281-8, v, 2002
17. Qureshi AI et al: Spontaneous intracerebral hemorrhage. N Engl J Med. 344(19):1450-60, 2001
P.II(1):17

Image Gallery

(Left) A 58-year-old male presented to his local ER with a severe headache. Initial outside NECT scan was read as normal

but showed a hyperdense right transverse sinus
. (Right) Two months later, the patient came to the ER with worsening
headache and acute onset of a left visual field defect. Repeat NECT scan now shows a focal right occipital hematoma
.

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