This document discusses the anatomy and ultrasound evaluation of veins in the upper extremity. It describes the cephalic, basilic, brachial, axillary, subclavian, and internal jugular veins. The technical procedure for venous doppler ultrasound is outlined, including patient positioning, scanning techniques, and diagnostic criteria. Potential pitfalls like rouleaux and limited windows are noted. Chronic changes after deep vein thrombosis like valve changes and collateral veins are also described. Ultrasound is useful for evaluating suspected deep vein thrombosis and mapping veins for dialysis access planning.
Role of medical imaging in management of arteriovenous fistula Dr. Muhammad B...Dr. Muhammad Bin Zulfiqar
This presentation is very helpful for vascular sergeons, interventional radiologists and sonographers that how to map Vasculature before construction of AV fistula for hemodialysis, how to check its patency, how to check its proper functioning ,to comment on its failure and decide when to reintervene.
Doppler ultrasound of visceral arteriesSamir Haffar
Doppler ultrasound of different diseases of visceral arteries including arterial stenosis and occlusion, arterial aneurysm, artrial pseudoaneurysm, arterio-venous fistula, artrial dissection, and abdominal vascular compression syndromes
Role of medical imaging in management of arteriovenous fistula Dr. Muhammad B...Dr. Muhammad Bin Zulfiqar
This presentation is very helpful for vascular sergeons, interventional radiologists and sonographers that how to map Vasculature before construction of AV fistula for hemodialysis, how to check its patency, how to check its proper functioning ,to comment on its failure and decide when to reintervene.
Doppler ultrasound of visceral arteriesSamir Haffar
Doppler ultrasound of different diseases of visceral arteries including arterial stenosis and occlusion, arterial aneurysm, artrial pseudoaneurysm, arterio-venous fistula, artrial dissection, and abdominal vascular compression syndromes
Peripheral artery diseases by Dr. Garvit.pptxgarvitnanecha
Peripheral artery disease seminar
Difference between artery and veins with detailed anatomy of arteries.
Peripheral pulses examination
Along with management including scores.
Differentials of blackening of hand and foot including management.
An educational PDF describing how to interpret Chest X-Ray. Common chest diseases radiographs are explained. An informative and useful material for every physician and medical student.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
3. • Superficial veins
1. Cephalic Vein
2. Basilic Vein
3. Median vein of
forearm
Deep veins
1. Brachial vein
2. Axillary vein
3. Subclavian Vein
4. Cephalic vein
• origin: radial aspect of the superficial
venous network of the dorsum of the
hand
• location: courses upwards on the
lateral aspect of the forearm and arm
• drainage: palm of the hand, lateral
aspect of the forearm and arm
• tributaries: median cubital vein and
accessory cephalic veins.
• Termination : medial aspect of the
axillary vein or the lateral aspect of
the subclavian vein
5. Basilic vein
• origin: ulnar aspect of the superficial
venous network of the dorsum of the
hand
• location: courses upwards on the
medial aspect of the forearm and
arm
• drainage: palm of the hand, medial
aspect of the forearm and arm
• tributaries: median cubital
vein and median antebrachial vein
• Termination : At the level of the teres
major muscle, it joins with the paired
deep brachial veins
6. Brachial vein
• origin: union of the ulnar and
radial veins in the cubital fossa
• location: courses superiorly in
the upper arm, often in close
proximity to the brachial
artery
• drainage: deep and superficial
palmar venous arches
• termination: union of the
brachial and basilic veins at
the inferior border of teres
major forms the axillary vein
7. Axillary vein
• origin: formed by the union of
the paired brachial veins and the
basilic vein
• location: courses medial and
superficial to the axillary artery in
the axilla
• drainage: upper limb, axilla and
superolateral chest wall
• tributaries: include the cephalic
vein and five other tributaries
which correspond to the
branches of the axillary artery
8. Subclavian vein
• starts at the crossing of the lateral
border of the 1st rib
• Arches cephalad, posterior to the
medial clavicle before curving caudally
and receiving its only tributary,
the external jugular vein
• joins the internal jugular vein
posterior to the sternoclavicular
joint, where it forms
the brachiocephalic vein
• The right and left brachiocephalic
veins merge to form the superior vena
cava, which subsequently enters the
right atrium.
9. • Perforating veins form important pathways of
collateralization in the presence of partial thrombosis.
• In the absence of thrombus they are typically too small
to see, but become more pronounced when they are
recruited to divert flow around a clot.
• Valves are present within the veins of the UE. As one
moves peripherally the location of the first valve is
quite variable, but typically is encountered in the
proximal brachial vein.
10. Advantages:
• Doppler study is a noninvasive imaging method
• B mode US combined with color flow doppler study provide
anatomical and physiological information as good as that
obtained with venography
• Relatively low cost
• Widely available
• Portabillity
• Proven high accuracy has lead to its primary role in diagnosis
of venous thrombosis
11. Disadvantages
• dependence on the skill of the operator
• technical difficulties in patients with oedema,
wounds or obesity
• low sensitivity for assessing DVT in the upper
thorax and arms (overlying skeleton, lungs and
large venous collateral pathways)
• difficulty in differentiatingrecanalized thrombus
from fresh thrombus
12. USES
• Evaluation of suspected DVT
• Evaluation of venous incompetence
• Preoperative vein mapping
• Evaluation of venous system for patency before
the placement of venous catheter
• For initial evaluation of vascular malformation.
15. Catheter-related thrombosis:
• caused by several factors.
• The vessel wall may be damaged during
catheter insertion or during infusion of
medication.
• Also, the catheter may impede blood flow
through the vein and cause areas of stasis
16. • Although the cause of upper extremity DVT
differs from that of the lower extremity, the
pathophysiology of its evolution is similar.
17.
18. • The sequelae of upper extremity thrombosis are less severe than
those of lower extremity thrombosis.
• Only 10% to 12% of patients with arm DVT develop pulmonary
emboli - majority of these are insignificant.
• manifestations of venous stasis and venous insufficiency caused by
DVT in the arm are less common and less severe than in the leg.
• Chronic swelling, skin changes, and nonhealing venous ulcers are
rare in the arm because of two major factors : extensive collateral
pathways and low hydrostatic pressure as compared to leg veins
19. Diagnostic Accuracy of Ultrasound
• The accuracy of ultrasound versus venography in
patients with acute DVT of the upper extremity has not
been studied as extensively as in the lower extremity.
• The available literature shows sensitivity ranging from
78% to 100% and specificity of 92% to 100%.
• The lower accuracy in the upper extremity compared
with the lower extremity is a result of the greater
number of technical challenges facing the examiner.
20. TECHNICAL PROCEDURES
• Similar principles to examination of lower extremity
venous examination:
- gray scale compression
- color Doppler
- spectral Doppler
• Typically, a 9-MHz linear array transducer – for internal
jugular vein and the arm veins through the axillary vein.
• 6-MHz transducer with color Doppler ultrasound capability
is often necessary to visualize the subclavian vein.
21. Positioning
• patient is positioned
supine, with the arm to
be examined slightly
abducted and rotated
externally.
• patient’s head is turned
slightly to the opposite
side
22. Scanning Technique
• Subclavian Vein
Patient supine on bed, arms by their side.
Scan in transverse at the antero-lateral base of
the neck.
A coronal, supraclavicular, inferiorly angled
approach is used medially, and a coronal,
infraclavicular, superiorly angled approach is
used laterally
Using colour doppler, find the Jugular vein and
follow inferiorly to the junction with the
subclavian vein.
Follow the subclavian vein laterally using
colour doppler in both longitudinal &
transverse planes to exclude non occlusive
filling defects.
23. • Internal jugular vein
examined initially with compression sonography in
the transverse plane and is followed inferiorly to its
junction with the subclavian and brachiocephalic
veins
An inferiorly angled, coronal, supraclavicular
approach- to evaluate the superior portion of the
brachiocephalic vein and the medial portion of the
subclavian vein.
Due to the proximity to the heart, duplex Doppler
spectral tracings in these sites will show greater
transmitted pulsatility than in the leg veins.
Loss of this pulsatility may be caused by a more
central venous obstruction .
24. • Axillary vein
Patient still supine on bed with
ipsilateral hand on their head, elbow
flexed laterally to permit easy access
to the axilla.
Find the distal subclavian artery and
follow through the axilla with colour
doppler and compression using b-
mode in the transverse plane
In the proximal arm, the axillary vein
will divide into the basilic and
brachial veins.
25. • Upper Arm Veins (Brachial & Basilic)
The basilic vein is the larger and is more
superficial. Usually single but may be
duplicated.
Continue from the axillary vein checking
in transverse that the basilic and
brachial veins of the upper arm are
compressible.
best acheived with the patient sitting on
the side of the bed with their arm
supinated.
At the antecubital fossa, the brachial
vein will divide into the radial & ulnar
veins.
26. • Forearm veins (Radial & Ulna)
Still with the patient seated on
the side of the bed, follow the
radial and ulnar veins to the
wrist confirming compressibility
and flow.
As with the veins in the calf, the
veins of the forearm generally
run in pairs (venous
commantantes)
27. Ultrasound and Compression
• Fresh thrombus may be extremely
hypoecoic – difficulty in visualization
- therefore, essential to perform
venous compression in a transverse
plane to rule out the presence of UE
DVT.
• Compression should be light
because fresh clots are soft and firm
pressure may give a false impression
of patency.
• cannot be used in portions of
subclavian vein and in the inominate
vein because of the overlying
structures – Color Doppler and
Spectral Doppler assessment
28. Ultrasound Color-Doppler
• As a result of right atrial contraction (a-wave) -pushes back
on venous return in the larger central veins- resulting in a
temporary reversal of flow. The color Doppler signal will
fluctuate in direction.
• With the pulse repetition frequency adjusted to a higher
level, the wall filter may suppress perception of slower
laminar flow along the wall, appearance that can be
confusing, mimicking a clot adherent to the wall.
• On the other hand, in the larger veins with the color-
Doppler pulse repetition frequency set relatively low, with
a brisk augment, aliasing may occur.
30. • If no thrombus occluding the vein- color spontaneously saturates
all lumen of the vessel.
• Because the veins of the UE are in close proximity to the heart, it is
normal to see a cardiac pulsatility in the spectral analysis.
• Spectral analysis of the caudal internal jugular vein and the medial
subclavian vein demonstrate central venous transmitted cardiac
pulsatility with a, c, v peaks, and x and y descents – rules out
obstruction
• In contrast to the lower extremity veins, the velocity of blood flow
in the veins of the upper extremity increases during inspiration
(inspiratory sniff) due to negative intrathoracic pressure and
increased venous return toward the heart.
31. • In a normal venous system there will be a
rapid rise and fall in the frequency shift,
whereas if there is a thrombosed venous
segment it will resist flow with damping or
absence of the augmentation response.
• squeeze should be rapid and not excessive –
risk of thrombus dislodgement.
32. In addition to the rapid phasic changes in cardiac pulsatility from atrial
contractions, there is a further variation in amplitude due to normal
respiratory variation.
35. Normal and abnormal response to sniff test.
A, Duplex spectral analysis of the internal jugular vein shows an increase in blood
flow velocity with inspiratory sniff, a normal response suggestive of central venous
patency.
B, Duplex spectral analysis of the contralateral internal jugular vein shows no increase
in blood flow velocity with inspiratory sniff, an abnormal
response suggestive of brachiocephalic or superior vena cava obstruction
37. Fig : A Gray-scale sonogram of the left internal jugular vein (arrows) in the transverse
view shows some echogenic material within it .
Fig B: Probe pressure is being exerted over the vein and the thrombus is preventing
the compression of the vein.
This is the key to positively identifying the presence of this non-occlusive thrombus
within the vein.
38. Triplex sonogram in the longitudinal view shows an occlusive thrombus in the
left axillary vein.
Patent segment below the clot demonstrates some slow anterograde
flow without respiratory variation or cardiac pulsatility.
39. POTENTIAL PITFALLS
1. Rouleaux
• Blood flow is anechoic because individual red blood cells are too
small to reflect the incoming sound wave.
• However, in certain conditions as infection, diabetes mellitus or
cancer, red blood cells may stick to each other, a finding that is
named rouleaux - aggregates are large enough to interact with the
insonating beam, manifesting as echoes in the bloodstream, and
are more likely to occur in areas of slow flow, especially in the sinus
behind the cusps of valves.
• If compression easily dislodges these Rouleaux aggregates,
presence of a clot is excluded.
40. Gray-scale sonogram in the longitudinal
view shows an area of slow flow in
the right internal jugular vein mimicking
deep venous thrombosis.
41. 2. Arm abduction
• Caution should be exercised in interpreting the distal subclavian
vein, which may appear falsely narrowed as it crosses between the
clavicle and the first rib at the thoracic inlet, due to complete
abduction of the upper extremity during examination.
3. Limited acoustic window
• due to bandages used to secure the catheters, radiation-induced
changes on the chest wall or the presence of indwelling catheters
4. Large venous collaterals
• In chronic obstruction, large venous collaterals often coexist and
can be misinterpreted as representing patent normal vessels.
42. CHRONIC CHANGES AFTER UEDVT
1. Valves
• If valve cusps appear rigid or fixed, this usually represents the
sequela of prior UEDVT.
2. Walls
• The walls of a normal vein are smooth and non obstructive.
• Following recanalization after DVT they become irregular,
thickened, echogenic and rarely calcified.
• Decreased diameter of venous lumina.
3. Venous collaterals
• Over a period of time the intramuscular venous channels expand
and become apparent on color Doppler.
43. Acute & chronic thrombus
Signs interpreted according to clinical history
• Anechoic or hypoechoic Brightly echogenic
• Homogenous Heterogenous
• Poorly attached or floating Well attached
• Smooth borders Irregular borders
• Spongy & deformable More rigid
• Increase in vein diameter Small & contracted vein
• Small collaterals Large collaterals
Acute thrombus Chronic thrombus
44. Ultrasound Venous Mapping for
Preoperative Planning of Dialysis Access
• non dominant arm first
• The vein mapped to receive the arterial anastomosis be measured after it is
dilated (use of sequential tourniquet placement or an inflated blood pressure cuff
on the arm) - closely approximates the size of the arterialized vein after fistula
formation.
• forearm vein most commonly used for AVF creation is the cephalic vein.
- assessed for compressibility, thrombus, and size
- minimal diameter of 0.25 cm for all veins used for an AVF
- measured at 7 to 8 sites on arm and forearm
• Veins must be relatively superficial to be easily cannulated after placement of a
fistula. The depth from the skin surface to the cephalic veins of adequate diameter
may be measured to assess the need for a subsequent superficialization
procedure.
45.
46. • If no suitable upper arm vein for AVF creation
is found, the largest brachial vein and the
axillary vein should be measured for potential
graft placement as previously described.
• A vein with a diameter of at least 0.4 cm is
needed for grafts
47. • Large branches of veins near the site of a fistula
can result in nonmaturation of the fistula. So, the
sites and sizes of vein branches may be noted.
• The internal jugular and subclavian veins should
be examined bilaterally to document symmetric
respiratory phasicity and transmitted cardiac
pulsatility as well as to exclude outflow stenosis.