Objectives of this presentation are
Introduction to ct
Cross sectional anatomy
Common important pathologies
This presentation is aimed to educate beginers to help in ct interpretetion.
Outlines of the presentation
- How to read a brain CT
- Gross CT brain anatomy
- Traumatic brain injury
- Ischemic and hemorrhagic strokes
- Type of intracranial hemorrhages
Objectives of this presentation are
Introduction to ct
Cross sectional anatomy
Common important pathologies
This presentation is aimed to educate beginers to help in ct interpretetion.
Outlines of the presentation
- How to read a brain CT
- Gross CT brain anatomy
- Traumatic brain injury
- Ischemic and hemorrhagic strokes
- Type of intracranial hemorrhages
Summary and illustrations of various traumatic brain injury including primary and secondary lesions as well as limited information on indications of brain imaging in trauma
Definition of stroke and cerebrovascular disorders and pathophysiology of cerebral infarct and CT imaging overview of acute-subacute and chronic infarcts and penumbra.
causes of cerebral edema , Radiological signs of acute infarct and hemorrhagic infarct and comparison of MRI and CT in the diagnosis of acute infarct
Role of diffusion weighted imaging (DWI) and diffusion perfusion mismatch
Summary and illustrations of various traumatic brain injury including primary and secondary lesions as well as limited information on indications of brain imaging in trauma
Definition of stroke and cerebrovascular disorders and pathophysiology of cerebral infarct and CT imaging overview of acute-subacute and chronic infarcts and penumbra.
causes of cerebral edema , Radiological signs of acute infarct and hemorrhagic infarct and comparison of MRI and CT in the diagnosis of acute infarct
Role of diffusion weighted imaging (DWI) and diffusion perfusion mismatch
in endo era. aortic is one of the industrial driven medical proedure & one of the most expensive. Its morbidity are quoet acceptable, but......... surgeon if the best deal behind this awsome techno
Current indications & therapies for Carotid Artery Stenosislpasek
Brought to you from the caring and expert staff of the beautiful modern Vascular Center at Sisters' of Charity Hospital of Buffalo, 2157 Main Street Buffalo, New York 14214 USA
General suggestions in ordering body CT in ED; vascular occlusion; aneurysm/pseudoaneurysm; bleeding and active contrast extravasation; extraluminal air
Practical Points in Emergency CT for Emergency PhysiciansRathachai Kaewlai
The handout describes some brief practical points on emergency CT, particularly for emergency physicians. They include imaging utilisation trends, radiation dose, contrast reaction, contrast-induced nephropathy, use of oral contrast medium and some caveats on emergency CT (esp. abdomen)
Five pearls and pitfalls in using head CT for diagnosis of traumatic brain injury. This was presented at the 51st Annual Scientific Meeting of the Royal College of Radiologists of Thailand (6 Aug 2014)
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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Decisions To Make
in Emergency Head CT
Prior to the scan During the scan After the scan
To perform or not How to perform Diagnosis
or differential diagnosis
How fast to perform IV contrast Recommendations
Any preparation needed Technique: CTA, CTV,
post-contrast imaging
Urgent findings needing
communication
Neck CTA as well?
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Scan Techniques
Non-contrast head CT
Acute stroke Trauma Trauma with spinal
board
Scan coverage Foramen magnum to vertex
Scan mode Conventional Helical Helical
Slice thickness 4 mm 3 mm 3 mm
kVp 120 120 120
mAs 300x0.75 200x0.75 220x0.75
Reformations Cor/sag 4 mm Ax/cor/sag bone 1 mm
Cor/sag 3 mm
Ax/cor/sag bone 1 mm
Cor/sag 3 mm
3D - Skull Skull
CTDIvol (mGy) 46.1 51.5 57
ACR CTDIvol upper limit (suggested): 75 mGy
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ICH: When To Stop at NCCT
SAH SDH IPH Multi-compartment
ICH
- Trauma and SAH
predominantly in
superficial location
- Any - Hypertension AND
IPH in one of these
locations:
Basal ganglia
Thalamus (unilateral)
Pons
Cerebellar hemisphere
- Trauma
Definitely
trauma
Definitely
hypertensive
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When Do We Need IV Contrast?
Clinical indications
• First-onset seizure
• R/O brain mass
• (R/O infection)
Non-contrast images
• Hemorrhage
– Lobar
– Non-traumatic SAH
– Deep SAH in trauma
• Hypodensity
– Not following arterial territories
– Vasogenic edema
• Normal non-contrast scan
– Hyperacute stroke <6 hr
– Suspected venous thrombosis
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Scan Techniques
Contrast-enhanced head CT
CT angiography/venography CT with IV contrast
Scan coverage Foramen magnum to vertex
Scan mode Helical Helical
Injection rate and
scan time
4 mL/s
CTA: trigger 120 HU at basilar artery
CTV: 25s after CTA or trigger 180 HU at sagittal sinus
1 mL/s, 70s
Slice thickness 1 mm 3 mm
kVp 120 120
mAs 280x0.75 200x0.75
Reformations MIP ax/cor/sag 5/3 mm
Small FOV at COW 0.5 mm
Cor/sag 3 mm
3D VRT -
CTDIvol (mGy) (no data) 51.5
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ICH: When To Do CTA
SAH SDH IPH Multi-compartment
ICH
- No trauma
- Trauma but SAH
predominantly in
deep location
- - Young patients
- Lobar Hemorrhage
in older patients
without known
malignancy
- No trauma
- No coagulopathy
Vascular diseases:
aneurysm, AVM
CTA spot sign
IPH = intraparenchymal hemorrhage
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ICH: When To Do CTV
Dural sinus thrombosis
During the Scan
SAH SDH IPH Multi-compartment
ICH
- - - Parasagittal, esp. if bilateral
- Bilateral thalamic
- Disproportionate surrounding
edema and no known malignancy
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When Do We Need Neck CTA?
• Stroke in the young (<40 yr)
– To R/O carotid/vertebral dissection (can be non-traumatic)
• Hyperacute stroke <6 hr if no bleeding seen on NCCT and
moderate/severe stroke
• Trauma to R/O arterial injuries: do neck CTA (covering circle of Willis
down to aortic arch)
– No need for head CTA
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ICH: CT vs MRI
NCCT
• Thought to be 100%
sensitive for detecing
“clinically relevant” acute
hemorrhage
• Criterion standard
MRI (Gradient imaging)
• GRE as sensitive as NCCT
for acute ICH
• More accurate for acute
stroke because better
sensitivity for ischemia
• Limited availability
• Contraindication
• Patient’s medical instability
• Operating time
Limit MRI usage
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CT Appearance of Hemorrhage
• CT attenuation links
to atomic number and
physical density of
globin molecules, and
hematocrit
Timing CT attenuation
<12 h Isodense,
heterogeneous
12h – 7d Hyperdense
7d – 1m Isodense
> 1m Isodense to hypodense
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MR Appearance of Hemorrhage
• Serum around clot will be bright on T2W
Blood products T1W T2W
Oxyhemoglobin I B
Deoxy Hb I (1-3 hr) D (2 hr)
Met Hb (in cells) B (3-14 hr) D
Met Hb (in solution) B B
Hemosiderin D D
B = bright, D = dark, I = isointense
I Be
IdDy
BidDy
BaBy
Doo Doo
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Clinical Diagnosis of ICH
• Often difficult
– Sudden onset focal neurological deficits, similar to patient with acute
ischemia
– Certain findings are more likely a/w ICH: LOC, coma, neck
stifness, seizure accompanying neurologic deficit,
dBP greater than 110 mmHg, vomitting, headache
• Many patients lack these features, neuroimaging is needed
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CT Often Sufficient for ICH
• Location of hemorrhage
• Unicompartmental or multi-??
• Secondary effect of hemorrhage
• Cause of hemorrhage
– Need IV contrast?
– CTA, CTV or routine post-contrast?
– MRI? MRA?
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Diagnosis & Differentials
Location Intra- or extra-axial
Supra- or infra-tentorial
Grey matter, white matter, deep nuclei
Specific structures
Anatomy
Appearance Hypo-, iso- or hyperdense
Enhancement
Acuity Acute, subacute or chronic History
Older exams
Secondary effects Effects to surrounding tissues
Brain herniations
Anatomy
Nature (Congenital)
Trauma
Tumor
Infection/inflammation
Vascular
Toxic/metabolic
Location
Appearance
Acuity
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Differentials by Location
SAH Aneurysm, trauma
Non-aneurysmal perimesencephalic SAH (pmSAH)
Brain AVM, DAVF, venous infarction, spinal AVM
EDH, SDH Trauma
For SDH in infants, consider non-accidental
IPH Hypertensive
Lobar
Vascular malformation
Tumor
Hemorrhagic venous infarct
Hemorrhagic transformation of ischemic infarct
Amyloid angiopathy
IVH Extension from IPH
Intraventricular tumor
Multicompartmental ICH Trauma, coagulopathy
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Subarachnoid Hemorrhage (SAH)
• Hemorrhage under the arachnoid membranes
• Worst headache of life
• Morbidity: vasospasm, mass effect (parenchymal
hematoma and hydrocephalus
• NCCT is probably best in acute setting
– Hyperdense sulci
• Probability of detection proportional to
– Amount of hemorrhage
– Time from hemorrhage onset
• NCCT sensitivity drops with time*
• 98-100% during first 12 hours
• 93% at 24 hours
• 57-85% at 6 days after onset
*Bederson JB, et al. Stroke 2009;40:994
SAH in cortical and cisternal
spaces. Arrow points to blood
reflux into ventricles
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Subarachnoid Hemorrhage (SAH)
• LP more sensitive than CT
• Negative NCCT but still suspicious of SAH –
still need LP
• MRI is sensitive to detect SAH using FLAIR, GRE
and SWI
– But problematic in perimesencephalic cistern
• Persistent vasospasm – vessels can be
permanently narrow
• Etiologies of non-traumatic SAH*
– 80% ruptured aneurysm
– 10% non-aneurysmal perimesencephalic SAH
– 10% others (brain AVM, spinal AVM, DAVF, venous
infarct, tumor)
Medscape.com
Cortical SAH on FLAIR (top) and
susceptibility (bottom) MR images
*Edlow JA, et al. J Emerg Med 2008;34:237
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Subarachnoid Hemorrhage (SAH)
• Scrutinize these areas systematically
for SAH
– Perimesencephalic cisterns
– Sylvian fissures
• Dilation of temporal horns suggestive
of hydrocephalus, which raises a
possibility of SAH
Lamina terminalis
cistern*
Interpeduncular
cistern
Quadrigeminal
cistern*
Sylvian cistern
Crural cistern
Ambient cistern
*Median, unpaired cisterns
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Subarachnoid Hemorrhage (SAH) and
Accompanying Hydrocephalus
• Common and may occur early
• May be obstructive or nonobstructive
– Plugging of cerebral aqueduct
– Plugging of arachnoid granulations decreased
uptake of CSF
• Earliest sign is dilation of temporal horns. must be
evaluated in all CTs
• Other findings: IVH, IPH, SDH
* *
* *
*
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SAH: Reversible Cerebral
Vasoconstriction Syndrome (RCVS)
• Reversible, multifocal cerebral vasoconstrictions
• Clinical thunderclap headache +/- neurodeficit
• NCCT often negative: 20% with small cortical SAH +/- IPH
• Vasculitic pattern on CTA, MRA and DSA
– Segmental arterial constriction
– Interval DSA may show rapid improvement with vasodilator Rx
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BEWARE: Cortical SAH from Venous
Sinus Thrombosis
Venous sinus thrombosis
Small SAH with hyperdense clot of superior sagittal sinus on CT, absence of flow voids on T2WI and
loss of venous signal on MRV image
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Hypertensive Hemorrhage
• Rupture of small blood vessel that has
been damaged by chronic HTN
• 50% of primary nontraumatic ICH
• Most common cause of spontaneous
ICH between 45-70 years
• Elderly patients a/w systemic HTN
• Predilection for areas supplied by
penetrating branches of MCA and
basilar arteries
– Putamen and external capsule 60-65%
– Thalamus 15-20%
– Pons, cerebellum10%
– Lobar 5-15%
*
Hypertensive hemorrhage of the right
putamen with mild surrounding edema
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Hypertensive Hemorrhage
• Neurologic deterioration common within 48 hr
– Increasing hematoma
– Edema
– Development of hydrocephalus
– Herniation syndromes
• Recurrent in 5-10% of cases usually in
different location
• 80% mortality in massive ICH with IVH *
Hypertensive hemorrhage in the left
thalamus and posterior limb of the left
internal capsule
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BEWARE: Some Basal Ganglia
Hemorrhage
• Young patient + No hypertension
Renovascular disease, pheochromocytoma, drugs, etc.
• Vascular malformation, aneurysm
• Hemorrhagic neoplasm
• Need IV contrast!
Basal ganglia hemorrhage secondary to reninoma.
Images from Mao J, et al. J Clin Hypertension 2012;14:802.
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Lobar Hemorrhage: Differentials
• Vascular (AVM, cavernous malformation), aneurysm
• Tumor
• Amyloid angiopathy
• Hemorrhagic venous infarct
• Hemorrhagic transformation of ischemic infarct
Lobar Hemorrhage a/w
subarachnoid extension is
unlikely related to HTN –
think vascular abnormalities.
Underlying cause of lobar hemorrhage
is often difficult to determine
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Arteriovenous Malformation (AVM)
• Pial vascular malformation of brain, artery
vein shunting. No intervening capillary bed
• “Young adult with nontraumatic ICH”
• All brain AVMs are potentially hazardous.
Majority becomes symptomatic
• Hemorrhage (50%), seizure (25%), focal
deficit (25%)
*
Hematoma of the left
parietotemporal lobe with edema
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Arteriovenous Malformation (AVM)
• NCCT: may be normal if small
– Iso-/hyperdense serpentine vessels
– Calcification in 25-30%
– If bleed, IPH, IVH >> SAH
• CECT: strong enhancement of arterial
feeders, nidus and draining veins
• CTA: enlarged feeders and draining veins
– Look for intranidal aneurysms
– Look for subtle early draining veins as a
clue to diagnose thrombosed AVM
• Main DDx: High-grade glioma with AV
shunting and dAVF
*
*
Two cases of AVMs presenting as lobar
hemorrhage. Arrows = AVM nidus
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Cavernous Malformation
• Far less frequent than AVM
• Lobulated collection of immature vessels,
hemorrhages of various stages without
normal intervening brain
• Cumulative risk of hemorrhage = 0.5-1%
per year (usually without clinical)
• 40-60 years, M = F
• Can enlarged, regress or occur de novo
• Size: microscopic to giant (> 6 cm)
• “Popcorn ball” on NCCT (neg in 30-50%)
• Little/no enhancement.
• CTA: usually negative
• Look for associated DVA
Cavernous malformation
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Bleeding Tumor
• Extensive and abnormal tumor vascularity
• Primary or metastatic tumors
• Metastatic disease
– Hemorrhage common with some mets
(melanoma, choriocarcinoma, lung, thyroid,
HCC, RCC)
– “Spontaneous” ICH in elderly patient may be
caused by metastasis
– Disproportionate surrounding edema
– Almost all enhance on CECT, mostly at rim
• High-grade glioma
– Most have marked vascularity +/- gross hemorrhage
– Necrotic core with thick, irregular enhancing tumor
most common in supratentorial white matter
– Marked mass effect and surrounding edema/tumor
infiltration
Bleeding metastatic tumor
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Hemorrhagic Venous Infarction
• Parenchymal abnormalities common with cortical venous thrombosis
– Petechial hemorrhage, edema
– Hypodensity in affected vascular distribution
• Many predisposing factors. No cause in 20-25%
• M < F, Most common presentation = headache
• Type 4 of venous ischemia (Type 1 = no abnormality, 2 = high T2/
FLAIR signal but no enhancement, 3 = high T2/FLAIR signal with
enhancement, 4 = hemorrhage or venous infarction)
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Hemorrhagic Venous Infarction
• Hyperdense cortical vein “cord” sign +/- dural sinus
thrombosis (DST)
• Enlarged veins (distended with clot)
• Linear, cigar-shaped thrombus
• Collateral channels and DST seen on CECT/CTV
• Negative CTV does not exclude CVT
– Nonocclusive thrombus
– Chronic thrombus (also enhances)
– Need to optimize technique (0.6 mm slice thickness,
MPr 1-2 mm with thick-slice overlaps
• NCCT is needed to exclude false-negative CTV
due to dense thrombus
– Bright dural sinuses may also be due to high HCT,
dehydration, polycythemia Superficial, lobar hemorrhage with SAH
and “empty delta” sign of the superior
sagittal sinus on post-contrast image
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Hemorrhagic Transformation of Ischemic
Infarct
• 15-20% of MCA occlusions
– Petechial hemorrhages: Punctate, increased
attenuation resulting in cortex appearing
“near-normal”
– Secondary hematoma: Discrete hematoma on
infarct, usually small component of
abnormal tissues
• Reperfusion of infarcted tissues which have
weakened vessels
• Usually by 48-72 hours after stroke onset
• Common location = basal ganglia and cortex
• Other signs of arterial ischemic infarct
– Wedge-shaped hypoattenuation involving both
gray and white matter
Diagram from Khatri R et al. Neurology 2012; 79:S52
Punctate hemorrhages seen
within right MCA infarct
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Cerebral Amyloid Angiopathy
• Degenerative blood vessels weakned by
deposition of B-amyloid
• Pathology: lobar hemorrhage, multiple
small cortical hemorrhages
• 10-20% localized form
• Usually in elderly
• “Normotensive demented patient with
lobar hemorrhage of different stages”
• Usually multiple, recurrent hemorrhages
with progressive cognitive decline
• Gray-white junction most commonly at
parietal and occipital lobes
• Not common in brainstem, deep gray
nuclei, cerebellum and hippocampus
Large lobar hemorrhage of the left temporal lobe without abnormal vessels or
enhancement. Susceptibility MRI showing several other microhemorrhages
**
*
*
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Unusual Causes of Lobar Hemorrhage
• Ruptured berry aneurysm
• Most intracranial aneurysm ruptures are a/w acute SAH but they
frequently have IPH
• Temporal region (MCA bifurcation aneurysm)
• Frontal region (AcoA aneurysm)
* *
MCA bifurcation aneurysm bleeds into the right temporal lobe
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CTA Spot Sign
• Prognostic sign in acute ICH suggesting
hematoma expansion
Findings
Appearance Serpiginous
Spot-like
Location Within margin of IPH
No connection to outside vessel
Size >1.5 mm diameter in maximal axial dimension
Density At least double the density (HU) compared to
background hematoma
Lesion number Multiple
Single
Thompson AL, Kosior JC, Gladstone DJ, et al. Can J Neurol 2009; 36:456.
*
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Intraventricular
Hemorrhage
• Blood in ventricular system
• Significant morbidity 2/2 obstructive
hydrocephalus
• Primary or secondary
– Primary – dominant blood in ventricles
(little, if any, parenchymal blood)
• Tumors or vascular malformations
– Secondary – large extraventricular
component (e.g., IPH or SAH with
secondary extension into ventricles).
• Far more common than primary
• In adults, this is commonly 2/2 basal ganglia
hypertensive IPH or SAH with ventricular reflux
• In children, this is a distinct entity SAH with ventricular reflux
*
*
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Communication of Urgent Findings
• Communication to referring physicians regarding “urgent” imaging
finding(s) is a standard of care
• Documentation of communication must be routine
• All ICHs are considered urgent findings – needing communication &
documentation
– New, increasing
– Except when it is known and stable from prior scan
• Be aware that many times, secondary effects are more catastrophic
than hemorrhages themselves
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Reading Emergency Head CT:
“Blood Can Be Very Bad”
Blood Evaluate for hemorrhage (bright white on CT)
Blood isodense around 1-2 weeks
Hypodense by 2-3 weeks
EDH, SDH, IPH, IVH, SAH and extracranial hemorrhage
Cisterns Four key cisterns examined for blood, asymmetry and effacement:
• Perimesencephalic
• Suprasellar
• Quadrigeminal plate
• Sylvian
Brain Look for symmetry, gray-white differentiation, shifting, hyper- or
hypodensity
Ventricles Hydrocephalus (first evident in dilation of temporal horns)
Compression/shift of ventricular system
Bone Fractures increase suspicion for intracranial injury
Perron AD. Emergency Medicine. Philadelphia, London: Saunders; 2008