Detailed presentation on Varicose veins, examination and management
Detailed presentation on Deep Vein Thrombosis, categories, staging and scoring systems and management.
Management also includes Endovascular and Surgical techniques.
Short notes made on IVC filters
Made by Ranjith R Thampi. A surgery powerpoint I made during internship for Management of Varicose Veins. Tried to cover as much as possible on the topic. Kindly comment before you download. Thanks!
Made by Ranjith R Thampi. A surgery powerpoint I made during internship for Management of Varicose Veins. Tried to cover as much as possible on the topic. Kindly comment before you download. Thanks!
This topic comes under the category - Venous Diseases. It is very important for a 3rd year MBBS Student to know about Varicose Veins, which is one of the commonest diseases encountered among out-patients.
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.
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.
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
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
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.
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.
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
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
3. Venous anatomy of lower limb
The venous system of the lower limb can be divided anatomically into
• the superficial venous system, which is located within the superficial tissues
• deep venous system, located deep to deep fascia and
• connected by fascial perforating veins.
5. Deep veins
• The deep veins of the lower limb
include three pairs of venae
commitantes, which accompany
the three crural arteries
• These six veins
intercommunicate and come
together in the popliteal fossa to
form the popliteal vein.
6. Fascial Perforators
Perforator Superficial vein Deep vein
Cockett’s Posterior arch
vein of
Leonardo
Posterior tibial
vein
Boyd’s Great
saphenous vein
Gastrocnemial
vein
Dodd Great
saphenous vein
Superficial
femoral vein
Hunterian Great
saphenous vein
Superficial
femoral vein
7. Pathophysiology of venous hypertension
• Venous return to heart is maintained by a pressure gradient between veins of leg and right
atrium.
• This is maintained by:
1. increase in thoracic volume during inspiration with a decrease in intrathoracic
pressure to -6 mm of Hg.
2. increase in the venous pressure by compression of the calf muscle pump
3. tone of the venous wall and
4. neuroendocrine factors.
8. Varicose Veins
• Varicose veins are dilated, tortuous elongated superficial veins ≥3 mm in diameter
measured in upright position with demonstrable reflux.
• There may be
• Primary varicose veins – idiopathic
• Secondary varicosities
9. Risk factors for primary varicose
veins
Risk factors for the development of varicose veins include
• Advancing age
• female gender
• Multiparity
• Obesity
• Heredity
• history of trauma to the extremity and
• prolonged standing.
10. Causes of secondary varicose veins
Pressure gradient dysfunction:
a. Increased abdominal or thoracic pressure:
1. COPD
2. Pregnancy
3. Obesity
4. Large tumour
5. Constipation
b. Decreased calf muscle pump function:
1. Immobility
2. Ankle joint fusion
3. Paralysis
Dysfunction of the venous system:
a. Venous structural deficit:
1. Valvular agenesis
2. Valvular incompetence
3. Venous dilatation
4. Loss of vein wall compliance and venous
tone
b. Venous occlusion by thrombosis
c. External venous compression:
1. May–Thurner syndrome
2. Pelvic/abdominal tumour
3. Pelvic/abdominal radiotherapy
11. Clinical features of venous hypertension
• Heaviness or aching in the leg present throughout day and increased by evening
• Discoloration
• Itching
• Cosmetic
12. Clinical features of venous hypertension
• Telangiectasia (spider veins): tiny intradermal venules less than 1 mm in diameter.
• Reticular vein: small dilated ‘bluish’ subdermal vein 1–2.9 mm in diameter.
• Varicose vein: subcutaneous dilated vein 3 mm in diameter or larger. They are elongated and
tortuous, with intermittent ‘blowouts’, and are defined by the presence of reflux.
• Saphena varix
• Corona phlebectatica (malleolar flare)
• Edema
• Eczema
13. Clinical features of
venous
hypertension
• Lipodermatosclerosis (LDS): chronic
inflammation and fibrosis of the skin and
subcutaneous tissues, resulting in a tight,
contracted, ‘woody’ leg on examination.
• Atrophie blanche: localized areas of
atrophic, white skin, often surrounded by
telangiectasia and pigmentation.
• Venous ulcer
14. Brodie - Trendelenburg’s test
• There are two components to this test. First, with the patient supine, the leg is elevated 45° to
empty the veins, and the GSV is occluded with the examiner’s hand or with a rubber
tourniquet. Then, with the GSV still occluded, the patient stands, the compression on the GSV
is released, and the superficial veins are observed for filling with blood.
• Sudden filling of veins on standing when GSV is released indicates incompetence of sapheno-
femoral junction .
• With the GSV still occluded, if there is filling of veins on standing for 1-minute, it indicates
incompetent perforators.
15. Tests for Varicose veins
Test Method and Interpretation
Morrissey’s test Cough impulse test
Modified Perthes test
Tourniquet is applied around the upper part of the thigh and patient is asked to walk
quickly with tourniquet in the place.
Severe crampy pain is suggestive of deep venous obstruction.
Schwartz test
In long standing varicose veins if the lower part of varicosity is tapped, an impulse is
felt at the saphenous opening.
Fegan's test
Palpation to find the fascial defects to locate incompetent perforators
16. Investigations
• Duplex ultrasonography (DUS) augmented by
color flow imaging is now the standard
diagnostic method in the evaluation of the
venous system.
• The scan should commence in the groin, using
a transverse view to identify the GSV and CFV
lying medial to the common femoral artery (the
‘Micky Mouse’ sign)
18. Treatment of Varicose veins
Varicose veins
treatment
Compression
dressing
Endothermal
ablation
Non-endothermal
non-tumescent
ablation
Catheter guided
sclerotherapy with
mechanical ablation
Foam Sclerotherapy
Open surgery
Saphenofemoral ligation and
great saphenous stripping
Saphenopopliteal junction
ligation and small saphenous
stripping
19. Compression dressing
• Compression dressing creates a graduated
external pressure of 30-40 mm Hg to
improve deep venous return and reduce
venous pressures.
• They significantly improves varicose vein
symptoms but has poor compliance and
long-term tolerance.
• They further will not prevent the
occurrence or progression of varicose
veins.
• Incorrect application of compression
hosiery can cause pressure necrosis,
tourniquet effects.
20. Endothermal ablation
• Endothermal ablation technologies replaced surgical ligation and stripping as the gold standard
treatment.
• It is cost effective as it can be performed as an outpatient procedure under local anesthetic.
• The basic concept is that a treatment device is inserted into the incompetent axial vein percutaneously.
• The vein is surrounded by tumescent local anesthetic solution causing:
1. compression of vein onto the treatment device, emptying it of blood.
2. hydro-dissects tissues such as nerves away from the zone of injury
3. it acts as a heat sink
21. Endothermal ablation
• The treatment device then
produces thermal energy
that destroys the structure of
the vein, resulting in
permanent occlusion.
• Two broad technologies
exist: laser and
radiofrequency ablation
23. Non-endothermal non-tumescent ablation –
Tessari Foam sclerotherapy
• This technique does not require tumescent anaesthesia.
• It involves injection of sclerosing agent into the vein.
• Sclerosing agents used are - Sodium tetradecyl sulfate, polidochanol and
ethanolamine.
• Destroys lipid membranes of endothelial cells causing them to shed, leading to
thrombosis, fibrosis and sclerosis.
• Foam sclerotherapy was developed as foam used will displace the blood from the
vessel and drug dose can be minimized.
24. Tessari Foam
sclerotherapy
• Sclerosant : air ratio is 1:3
or 1:4.
• Complications:
• Anaphylaxis
• Thrombophlebitis
• Thrombosis
• Skin ulceration
• Skin discoloration
25.
26. Catheter guided sclerotherapy with
mechanical ablation
• This involves deployment of a catheter within the vein lumen and an angled wire
attached to a motorized handle is inserted from the end.
• The trigger on the handle is depressed, spinning the wire around and liquid
sclerosant is infiltrated via the catheter simultaneously during catheter withdrawal.
• The spinning wire causes physical damage to the endothelium and deeper
penetration of the sclerosant into the vein wall.
27. Open Surgery -
Saphenofemoral
ligation & vein
striping
Saphenofemoral ligation and great
saphenous stripping:
• An oblique groin incision made just lateral to pubic
tubercle
• Long saphenous vein identified and dissected till SFJ.
• 6 tributaries identified and ligated.
• Flush ligation of GSV done followed by striping of the
vein to the knee. .
Complications:
• Bleeding
• Postoperative pain
• Permanent skin discoloration
• Saphenous nerve injury
28. Minimally invasive surgery
Sole incompetent perforators or distal perforators following junctional ligation are
managed by:
1. Conventional phlebectomy (stab avulsion)
2. Powered phlebectomy
3. Subfascial endoscopic perforator vein surgery (SEPS)
29. Recurrence of Varicose veins
Recurrence is due to:
1. Neovascularization
2. Reflux in residual axial vein
3. Inadequate ligation
4. New junctional reflux
31. Deep Vein Thrombosis - epidemiology
• Deep vein thrombosis (DVT) and venous thromboembolism (VTE), remain an
important preventable cause of morbidity and mortality in a surgical patient.
• The incidence of VTE is approximately 100 per 100,000 people per year in
the general population, with 20% of the diagnoses made within 3 months
of a surgical procedure.
32. Deep Vein Thrombosis - epidemiology
• Of the symptomatic patients, one-third will present with PE and two-thirds
with DVT.
• Acute DVT poses several risks and has significant morbid consequences viz.,
edema, pain, immobility and the most dreaded sequel of pulmonary embolism.
33. Etiopathogenesis of DVT – Virchow’s Triad
Virchow’s
triad of
thrombosis
Circulatory
stasis
Hypercoag
ulability
Vascular
damage
34. Etiopathogenesis of DVT
• Of these risk factors, relative hypercoagulability appears most
important in cases of spontaneous VTE, or so-called idiopathic
VTE, whereas stasis and endothelial damage likely play a
greater role in secondary VTE.
35. Etiopathogenesis of DVT – stasis and
vascular damage
• The stasis may contribute to the endothelial cellular layer contacting
activated platelets and procoagulant factors, thereby leading to DVT.
• Though overt loss of endothelium exposing subendothelial ECM, is
required for thrombus formation, endothelium need not be denuded or
physically disrupted to contribute to the development of thrombosis; any
perturbation in the dynamic balance of the prothrombotic and
antithrombotic effects of endothelium can influence clotting locally.
36. Etiopathogene
sis of DVT –
hypercoagula
bility
Primary (genetic) causes:
• Factor V Leiden
• Prothrombin
20210A
• Antithrombin
deficiency
• Protein C deficiency
• Protein S deficiency
• Factor XI elevation
• Dysfibrinogenemia
Mixed causes:
• Antiphospholipid
antibody
syndrome
• Homocysteinemi
a
• Factors VII, VIII,
IX, XI elevation
37. Secondary (acquired) causes of DVT
Advanced age
Hospitalization/immobilization
Hormone replacement therapy & OC pills usage
Pregnancy and puerperium
Prior venous thromboembolism
Malignancy
Major surgery
Obesity
Nephrotic syndrome
Trauma or spinal cord injury
Varicose veins
Polycythaemia
38. Diagnosis of DVT – clinical evaluation
• Diagnosis of DVT requires a high index of suspicion.
• Usually, there may be no or few clinical findings such as pain,
swelling or erythema.
• On examination there may be tenderness, erythema and dilated
superficial veins with Homan’s sign being positive occasionally.
• History and physical examination are often nonspecific and
unreliable.
41. Pre-test probability – modified WELL’S
scoring
Variable Score
Lower limb trauma or surgery or immobilization in a plaster cast 1
Bedridden for >3 days or surgery in last 4 weeks 1 1
Previous DVT 1
Malignancy (including treatment up to 6 months ago) 1
Pitting edema 1
Dilated collateral superficial veins (not varicose veins) 1
Entire limb swollen 1
Tenderness along the line of femoral or popliteal veins 1
Calf circumference >3 cm than the other side (10 cm below the tibial tuberosity) 1
Intravenous drug abuse 3
Alternative diagnosis more likely than DVT -2
42. Clinical suspicion of DVT – Modified wells scoring
Suspicion unlikely (score ≤2)
D-dimer
Normal
Diagnosis ruled out
Raised
Duplex ultrasound
Likely DVT (score >2)
Duplex ultrasound
43. Diagnosis of DVT –
Duplex ultrasound
• Most commonly performed test for
the detection of DVT.
• Uses real-time B-mode ultrasound
with compression and flow
augmentation amneuvres combined
with venous Doppler.
• It is a non-invasive method -
visualizing venous anatomy, detecting
completely and partially occluded
venous segments, and demonstrates
physiologic flow characteristics.
44. Diagnosis of DVT – Fibrinogen Uptake (FUT)
• Iodine-125 fibrinogen uptake (FUT) involves IV administration of
radioactive fibrinogen and monitoring for increased uptake in
fibrin clots.
• An increase of 20% or more in one area of a limb indicates an
area of thrombus.
• FUT can detect DVT in calf, but high background radiation from
pelvis and urinary tract limits its ability to detect proximal DVT.
• It also cannot be used in an extremity that has recently
undergone surgery or has active inflammation.
45. Diagnosis of DVT - Venography
• Venography is the gold standard method.
• Done by placing a small catheter in a dorsal
foot vein and a radiopaque contrast agent is
injected. Radiographs are obtained after
injection.
• A positive test result is failure to fill the deep
system with passage of the contrast medium
into the superficial system or demonstration of
filling defects.
• A normal study result virtually excludes the
presence of DVT.
46. Differential diagnosis of DVT
• Cellulitis
• Lymphoedema
• Chronic venous insufficiency
• Haematoma and
• Ruptured Baker cyst.
47. Treatment of DVT
• Anticoagulation is the mainstay of treatment for DVT and patient
with confirmed DVT on duplex imaging should be anticoagulated
rapidly.
• The aim of it is to reduce mortality, thrombus extension,
recurrence, and the risk of PTS (after DVT) and chronic
thromboembolic pulmonary hypertension (after pulmonary
embolism).
48. Various anticoagulants
Anticoagulant Indications Dose Route Adverse effects Monitoring
Contraindica
tions
Reversal agent
Unfractionated
heparin
• DVT
• PE
• Cancer-
associated
VTE
80 IU/
kg
intravenous
bolus, then
18 IU/
kg per hour
IV
infusion
PTT
at 60 to 80
seconds
Heparin-
induced
thrombocytop
enia
Protamine
Warfarin
• DVT
• PE
Typically
start with
5mg
Oral
Bleeding,
intracranial
haemorrhage,
not
safe in
Pregnancy
target INR
2.0–3.0
Intracranial
haemorrhage,
skin
necrosis,
pregnancy,
breastfeeding
Vitamin K,
prothrombin
complex
concentrate
49. Various anticoagulants
Anticoagulan
t
Indications Dose Route
Adverse
effects
Monitorin
g
Contraindications
Reversal
agent
Rivaroxaban
1. DVT
2. PE
15 mg oral
twice daily
for 21 days,
then 20 mg
daily
Oral Bleeding No
Severe renal and hepatic
impairment, pregnancy,
breastfeeding
Enoxaparin
1. DVT
2. PE
3. Cancer-
associated
VTE
Typically
start with
5mg
Oral Bleeding No
Heparin-induced
thrombocytopenia
within previous 100 days
Dabigatran
1. DVT
2. PE
150 mg oral
twice
daily
Oral
Bleeding,
dyspepsia No
Severe renal and hepatic
impairment, pregnancy,
breastfeeding
Idarucizu
mab
50. Duration of anticoagulation
Subgroup Duration of anticoagulation
proximal DVT provoked
1. by surgery or trauma
2. by a non-surgical transient risk factor
3. unprovoked isolated distal DVT and
4. for unprovoked DVT when the bleeding risk is high
3 months
DVT provoked by active cancer 6 months
1. recurrent DVT
2. for unprovoked proximal DVT when the bleeding risk is low
Extended anticoagulation
51. Treatment of DVT - Thrombolysis
• Catheter-directed thrombolysis (CDT) involves the percutaneous
insertion of a catheter and infusion of a thrombolytic typically
recombinant tissue plasminogen activator (tPA) directly into the
thrombus.
• There is no reduction in the risk of post-thrombotic syndrome (PTS)
but has increased bleeding risk.
• Indications – extensive iliofemoral DVT and phlegmasia cerulea
dolens.
52. IVC filters
• Indications of IVC filters include:
• manifestations of lower extremity VTE and
absolute contraindications to anticoagulation,
• patients having bleeding complication from
anticoagulation therapy of acute VTE
• who develop recurrent DVT or PE despite
adequate anticoagulation therapy and
• for patients with severe pulmonary
hypertension
53. IVC filters
Remove IVC
filterswithin 29 and 54
days after
implantation.
Complications include
thrombosis or bleeding
at the insertion site
misplacement of the
filter
thrombosis of the IVC,
DVT,
breaking, migration
Erosion of the filter
through the IVC.
54. Treatment of DVT – Surgical thrombectomy
• Surgical therapy is generally reserved for patients
1. worsening with anticoagulation therapy
2. phlegmasia cerulea dolens and
3. impending venous gangrene
• Patient with phlegmasia cerulea dolens - a fasciotomy.
• In iliofemoral DVT - a longitudinal venotomy in the common femoral vein with
venous balloon embolectomy of proximal thrombus and manual pressure removal
of distal thrombus with application of a tight rubber elastic wrap.
55. Treatment of
DVT –
Surgical
thrombectomy
For a thrombus extending into
IVC - IVC exposure
transperitoneally and thrombus
removal by gentle massage.
Every operated patient should
be anticoagulated with heparin
for several days.
58. Thromboembolism risk and recommended
thromboprophylaxis in surgical patients
LEVEL OF RISK
APPROXIMATE DVT RISK
WITHOUT
THROMBOPROPHYLAXIS
SUGGESTED
THROMBOPROPHYLAXIS
OPTIONS
Very low risk general or
abdominopelvic surgery
<0.5% (Rogers score <7;
Caprini score 0)
No specific thromboprophylaxis
Early ambulation
Low-risk general or
abdominopelvic surgery
∼1.5% (Rogers score 7–10;
Caprini score 1–2)
Mechanical prophylaxis
Moderate-risk general or
abdominopelvic surgery
∼3.0% (Rogers score >10;
Caprini score 3–4)
LMWH (at recommended doses),
LDUH, or mechanical prophylaxis
High-risk general or
abdominopelvic surgery
∼6% (Caprini score ≥5)
LMWH (at recommended doses),
fondaparinux and mechanical
prophylaxis
60. Duration of prophylaxis
• Thromboprophylax
is should be
continued until
discharge
Drug Dose and route Comment
Low dose
unfractionated
heparin
5000 IU 8-12hly;
subcutaneously
Maybe started 12
hours before
surgery
Enoxaparin 40mg once a day;
subcutaneously
Maybe started 12
hours before
surgery