This document discusses venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE). It covers the pathophysiology of VTE involving Virchow's triad of venous stasis, endothelial injury, and hypercoagulability. Evaluation and diagnostic methods are described, including clinical assessment, d-dimer testing, ultrasound, CT, lung scanning, and angiography. Management includes anticoagulation with unfractionated heparin, low molecular weight heparin, fondaparinux, vitamin K antagonists, and direct thrombin inhibitors. Outcomes of both DVT and PE such as post-thrombotic syndrome and mortality are addressed
Deep vein thrombosis (DVT), is the formation of a blood clot in a deep vein, most commonly the legs.[2][a] Symptoms may include pain, swelling, redness, or warmth of the affected area. About half of cases have no symptoms. Complications may include pulmonary embolism, as a result of detachment of a clot which travels to the lungs, and post-thrombotic syndrome.[2][3]
Risk factors include recent surgery, cancer, trauma, lack of movement, obesity, smoking, hormonal birth control, pregnancy and the period following birth, antiphospholipid syndrome, and certain genetic conditions. Genetic factors include deficiencies of antithrombin, protein C, and protein S, and factor V Leiden mutation. The underlying mechanism typically involves some combination of decreased blood flow rate, increased tendency to clot, and injury to the blood vessel wall.
It is estimated that 20% of American women and 7% of American men suffer from venous disease. Venous disease results in symptoms such as aching, fatigue, swelling, and pain in the legs which can interfere with daily living.Cosmetic issues may affect quality of life.
At least 20% of patients with venous disease will develop leg ulcers. This presentation outlines the normal anatomy and physiology of venous drainage of the extremities as well as the common venous disorders such as varicose veins and deep vein thrombosis.
Deep vein thrombosis (DVT), is the formation of a blood clot in a deep vein, most commonly the legs.[2][a] Symptoms may include pain, swelling, redness, or warmth of the affected area. About half of cases have no symptoms. Complications may include pulmonary embolism, as a result of detachment of a clot which travels to the lungs, and post-thrombotic syndrome.[2][3]
Risk factors include recent surgery, cancer, trauma, lack of movement, obesity, smoking, hormonal birth control, pregnancy and the period following birth, antiphospholipid syndrome, and certain genetic conditions. Genetic factors include deficiencies of antithrombin, protein C, and protein S, and factor V Leiden mutation. The underlying mechanism typically involves some combination of decreased blood flow rate, increased tendency to clot, and injury to the blood vessel wall.
It is estimated that 20% of American women and 7% of American men suffer from venous disease. Venous disease results in symptoms such as aching, fatigue, swelling, and pain in the legs which can interfere with daily living.Cosmetic issues may affect quality of life.
At least 20% of patients with venous disease will develop leg ulcers. This presentation outlines the normal anatomy and physiology of venous drainage of the extremities as well as the common venous disorders such as varicose veins and deep vein thrombosis.
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!
1) Review of the Evidence on Diagnosis of Deep Venous Thrombosis and Pulmonary Embolism
2) Duration of anticoagulant therapy after a first episode of an unprovoked pulmonary embolus or deep vein thrombosis
PERIPHERAL ARTERIAL DISEASES- INTRODUCTION- Limb Ischemia
Dear Viewers,
Greetings from “Surgical Educator”
Today I am uploading an introductory video on “Peripheral Arterial Diseases”. In this video I have discussed the surgical anatomy, modes of presentation, symptoms, signs, investigations and a diagnostic algorithm of Peripheral Arterial Diseases. In the subsequent three videos I will discuss about chronic lower limb ischemia, acute lower limb ischemia and upper limb ischemia. I hope you will enjoy these series of teaching videos. You can watch these videos in the following links:
surgicaleducator.blogspot.com
youtube/c/surgicaleducator
Thank you for watching the video.
anatomy of the lower extremity veins, CVI , ambulatory venous hypertension, varicose veins , clinical examination and performance of various tests of the varicose veins
DEEP VEIN THROMBOSIS- Venous Diseases
• Dear Viewers,
• Greetings from “Surgical Educator”
• Today I have uploaded a video on Deep Vein Thrombosis- DVT
• In this video I discussed about the etio-pathogenesis, clinical features, investigtions, Wells scoring, differential diagnosis and treatment both prophylactic and definitive of Deep Vein Thrombosis.
• I hope you will enjoy the video.
• You can watch all my teaching videos in the following links:
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video
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!
1) Review of the Evidence on Diagnosis of Deep Venous Thrombosis and Pulmonary Embolism
2) Duration of anticoagulant therapy after a first episode of an unprovoked pulmonary embolus or deep vein thrombosis
PERIPHERAL ARTERIAL DISEASES- INTRODUCTION- Limb Ischemia
Dear Viewers,
Greetings from “Surgical Educator”
Today I am uploading an introductory video on “Peripheral Arterial Diseases”. In this video I have discussed the surgical anatomy, modes of presentation, symptoms, signs, investigations and a diagnostic algorithm of Peripheral Arterial Diseases. In the subsequent three videos I will discuss about chronic lower limb ischemia, acute lower limb ischemia and upper limb ischemia. I hope you will enjoy these series of teaching videos. You can watch these videos in the following links:
surgicaleducator.blogspot.com
youtube/c/surgicaleducator
Thank you for watching the video.
anatomy of the lower extremity veins, CVI , ambulatory venous hypertension, varicose veins , clinical examination and performance of various tests of the varicose veins
DEEP VEIN THROMBOSIS- Venous Diseases
• Dear Viewers,
• Greetings from “Surgical Educator”
• Today I have uploaded a video on Deep Vein Thrombosis- DVT
• In this video I discussed about the etio-pathogenesis, clinical features, investigtions, Wells scoring, differential diagnosis and treatment both prophylactic and definitive of Deep Vein Thrombosis.
• I hope you will enjoy the video.
• You can watch all my teaching videos in the following links:
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video
Its a elaborate presentation on deep vein thrombosis by surgery resident.
Inform me if any thing needed to be correction.
thank you.
Dr Syed Aftub Uddin, MBBS,CCCD, MS ( Resident)
email: aftub_16@yahoo.com
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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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.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
2. Major cause of morbidity and mortality in the
hospitalized patient, particularly in the surgical patient.
The triad of venous stasis, endothelial injury, and
hypercoagulable state first posited by Virchow in 1856
3. The most dreaded sequel to acute DVT is that of
pulmonary embolism, a condition of potentially lethal
consequence.
The late consequence of DVT, particularly of the
iliofemoral veins, can be CVI and ultimately post-
thrombotic syndrome, as a result of valvular
dysfunction in the presence of luminal obstruction
4. Hepercoagulbility-
Most impotant in most cases of spontaneous VTE (Idiopathic
VTE)
Stasis and endothelial damage
Greater role in secondary VTE( provoked VTE)
Occurs in association with risk factors like immobilasation,
surgical procedures and trauma
5. The Hypercoagulable State
Factor V Leiden mutation
Prothrombin gene mutation
Protein C deficiency
Protein S deficiency
Antithrombin III deficiency
Homocysteine
Antiphospholipid syndrome
6. After major operations
Damaged tissue tissue factor may be released into the
bloodstream
potent procoagulant expressed on the leukocyte cell surface as
and as soluble form in the bloodstream
•Increases in platelet count,
•adhesiveness,
•changes in coagulation
cascade,
•endogenous fibrinolytic
activity
Thrombosis
7. Stasis
soleal sinuses are the most common sites of initiation
of venous thrombosis.
stasis may contribute to the endothelial cellular layer
contacting activated platelets and procoagulant
factors, thereby leading to DVT.
Stasis, in and of itself, has never been shown to be a
causative factor for DVT.
8. Venous Injury
venous thrombosis occurs in veins that are distant from the site
of operation
multiple microtears noted within the valve cusps that resulted in
the exposure of the subendothelial matrix
9. Initial Evaluation
1. Approximately 75% of patients with suspected DVT
or PE turn out not to have these condition
2. Assessment of Risk factor
10. Initial Evaluation
3. Clinical presentation
• Extremity pain
• Increased cicumference with respect to
contralateral extremity
• Dilatation of supeficial veins of suspected
extremity only
11. • Phlegmasia cerulea dolens
o Extensive DVT of major axial deep venous channels
o Relative sparing of collaterals
o Pain, pitting oedema and cyanosis
• Phlegmasia alba dolens
Thrombous extension to collateral system
Massive fluid sequestrationsignificant oedema
Extremely painful and oedematous, pale secondary
to arterial insufficiency increases in below in
compartment pressue
13. Assessing Clinical likelyhood
Clinical Variable Score
Active cancer 1
Paralysis, paresis, or recent cast 1
Bedridden for >3 days; major surgery
<12 weeks
1
Tenderness along distribution of deep
veins
1
Entire leg swelling 1
Unilateral calf swelling >3 cm 1
Pitting edema 1
Collateral superficial nonvaricose veins 1
Alternative diagnosis at least as likely
as DVT
–2
Low Clinical Likelihood of DVT if Point Score Is Zero
or Less
Moderate-Likelihood Score Is 1 to 2
High-Likelihood Score Is 3 or Greater
14. Assessing Clinical likelyhood
Clinical Variable Score
Signs and symptoms of DVT 3.0
Alternative diagnosis less likely than PE 3.0
Heart rate >100/min 1.5
Immobilization >3 days; surgery within 4
weeks
1.5
Prior PE or DVT 1.5
Hemoptysis 1.0
Cancer 1.0
High Clinical Likelihood of PE if Point Score Exceeds
4
15. Nonimaging Diagnostic Modalities
Blood test
D-Dimer rises in the presence of DVT or PE because of the
breakdown of fibrin by plasmin.
The sensitivity of the d-dimer is >80% for DVT (including
isolated calf DVT) and >95% for PE.
The d-dimer is less sensitive for DVT than for PE because
the DVT thrombus size is smaller.
The d-dimer is a useful "rule out" test.
More than 95% of patients with a normal (<500 ng/mL) d-
dimer do not have PE.
16. • The d-dimer assay is not specific.
Levels increase in patients with
myocardial infarction,
pneumonia, sepsis,
cancer,
the postoperative state
those in the second or third trimester of pregnancy.
• Therefore, d-dimer rarely has a useful role among
hospitalized patients, because levels are
frequently elevated due to systemic illness.
19. USG rules out other D/ds
Baker's cyst (also known as a popliteal or synovial
cyst
hematoma
technically poor or nondiagnostic venous
ultrasound alternative imaging modalities CT
and MRI
20. Duplex ultrasound
Real time B mode USG +pulse doppler capability
Lack of spontaneous flow
Incompressibility
Absence of color filling of lumen by color flow DUS
Loss of respiratory flow variation and venous
distension
21. Chest CT
RV enlargement on chest CT indicates an
increased likelihood of death within the next 30
days compared with PE patients who have
normal RV size on chest CT.
imaging is continued below the chest to the
knee pelvic and proximal leg DVT also can be
diagnosed by CT scanning.
Rules out other
pneumonia, emphysema, pulmonary fibrosis,
pulmonary mass, and aortic pathology.
22. Lung Scanning
second-line diagnostic test for PE
used mostly for patients who cannot tolerate intravenous
contrast
Small particulate aggregates of albumin labeled with a
gamma-emitting radionuclide are injected intravenously
and are trapped in the pulmonary capillary bed
perfusion scan defect indicates absent or decreased
blood flow, possibly due to PE.
Ventilation scans, obtained with a radiolabeled inhaled
gas such as xenon or krypton, improve the specificity of
the perfusion scan.
23. A high-probability scan for PE is defined as one
that indicates two or more segmental perfusion
defects in the presence of normal ventilation
24. Magnetic Resonance (MR)
suspected VTE patients with renal insufficiency or
contrast dye allergy.
may detect large proximal PE but is not reliable for
smaller segmental and subsegmental PE.
25. Echocardiography
useful diagnostic tool for detecting conditions that
may mimic PE, such as acute myocardial infarction,
pericardial tamponade, and aortic dissection
The best-known indirect sign of PE on transthoracic
echocardiography is McConnell's sign: hypokinesis
of the RV free wall with normal motion of the RV apex
26. Pulmonary angiography
technically unsatisfactory chest CTs
interventional procedure such as catheter-directed
thrombolysis or embolectomy is planned.
visualization of an intraluminal filling defect in more
than one projection.
Secondary signs of PE include abrupt occlusion
("cut-off") of vessels, segmental oligemia or
avascularity, a prolonged arterial phase with slow
filling, and tortuous, tapering peripheral vessels.
27. Management
Goal of VTE Management
Prevention of mortality and morbidity associated
with PE and prevention of post thrombotic
syndrome
Treatment option
Antithrombotic therapy
Temporary or permanent venacaval filter placement
Catheter directed or systemic thrombolytic therapy
Operative thrombectomy
28. Antithrombotic therapy
IV or SC UFH
SC LMWH
Foundaparinux
Warfarin
Begun after initiation IV/SC therapy
IV/SC continued until oral anticoagulatio achieved
( INR>2)
Minimum 5 days of heparin or fondaparinux recommended
29. UFH
Binds to antithombin III
inhibits factor IIa ( Thrombin) and facto Xa and also F
IXa,XIa and XIIA of coagulation cascade
Dose-
IV bolus- 80u/kg
Followed by continious IV drip at 18units/kg/hr
T1/2- 45-90min (dose dependent)
Monitoring- aPTT 6hourly
aPTT goal- 1.5 to 2 times the control value
30. Complication of UFH
1.Hemorrahage
Fatal, intracranial hemorrhage, retroperitoneal or
requiring >2 unit of packed red cell is aprox 5 % in
hospitalized patient
Management
Discontinue UFH
Protamine sulphate
1mg protamine neutralizes 90-115 unit of heparin
Dose not to exceed 50mg IV over any 10 min
31. Protamine sulphate side effect
Hypotension
Pulmonary edema
Anaphylaxis
Patient on NPH and allergic to fish
32. Complication of UFH
2. HIT
Results due to heparin associated antiplatelets
antibody complex
Repeted heparin exposure( vascular Sx- 21%)
Occurs m/c in 2nd week of therapy
Platelet counts to be monitored periodically
Dx- exposure to Heparin + platelets <100,000 and/ or
decline in 50% of platelet following exposure
33. Complication of UFH
3. Heparin induced osteopenia
impairment of bone formation and enhancement of
bone resorption by heparin
34. LMWH(enoxaparin)
Derived from polymerization of porcine UFH
Act more on F Xa
Increased bioavailability
2-4 times longer half life
Can be administered S.C without lab monitoring
Partially reversible by protamine (60%)
Patient requiring monitoring
Severe renal impairment, pediatrics,pregnants, wt>120kg
HIT <2%
Established HIT- not be used
Outpatient treatment
Reduce hospital stay
35. Fondaparinux
Synthetic petasaccharide
Activated antithrombin and Xa inhibiion
Recurrent VTE- 3.8-5%
Major bleeding- 2-2.6%
Administered – SC once daily dose
Half life 17 hour
36. Direct thrombin inhibitors
Hirudin,argatroban and bivalirudin
Binds thrombin and inhibiting conversion of fribrinogen to
fibrin and fribrin induced thrombocytopenia
Used for high suspicion/confirmed HIT or with
history of HIT or HAAb positive cases
Requires aPTT adjustment
37. Vitamin K antagonist
Main stay of long term antithrombotic therapy
Warfarin and other coumarin derivatives
Inhibits gamma carboxyaltion of Vit K dependent factors and
protein C and S
Requires several days to achieve full effect ( 4-5 days)
Monitored by INR
INR= (patient PT/lab normal PT)*ISI
ISI- international senstivity index- strength of thromboplastin
that is added to activate the extrinsci coagualtion pathway
38. warfarin
Therapeutic range- 2-3
To be started on same day of starting parenteral
anticoagualation ( except with concominant thrombolysis
and venous thrombectomy)
Usual starting dose 50-10mg
Smaller dose for older, malnourished, liver disease and
CHF
Variability of response
Depends upon Liver funtion, diet, age and medicaitons used
41. Systemic and catheter directed
lysis(CDT)
Indication
Extensive proximal, iliofemoral DVT
Streptokinase
B-hemolytic streptococcus
Acute MI,PE,DVT, arterial thromboembolism, occulded
central lines
Limited use- antigenicity (fever/shiver-1-4%)
Urokinase
Human neonatal kidney
Alteplase,reteplase
Recombinant variants of tissue plasminogen activator
CDT of DVT, PE, acute MI
42. Systemic thrombolysis/ CDT
Systemic thrombolysis
More clot lysis
Less PTS
More bleeding complication
CDT
Administer lytic agent alone
Pharmacomechanical clot lysis
43. Inferior Venacaval filters
Patients with proven VTE with
contraindication for anticoagulation
complication of anticoagulation
or recurrent VTE despite of anticoagulaiton
44. Operative thrombectomy
ileofemoral DVT
Worsening with anticoagulation therapy
Phlegmasia cerulea dolens
Impending venous gangrene
Pulmonary thormobectomy
Massive pulmo emboli with failed thrombolysis or
contraindication to thrombolytics
Posterolateral thoracotomy
Percutaneous catheter based technique- mechanical
clot fragmentation followed by CDT
46. Elastic compression stockings
Assist calf muscle pump and reduce venous
hypertension and venous valvular reflux
Reduces leg edema, aids the microcirculaiton,
prevents ischemia
Regular use of ECS reduced the Post thrombotic
syndrome by 50%
30- to 40-mmHg vascular compression
When patients are in bed, the stockings need not be
worn
47. Ambulation
ACCP Concensus Conference on antithrombotic and
thrombolytic therapy for VTE (2012)
Ambulation as tolerated for patient with DVT
Early ambulaiton on day 2 after initiation of outpatient anticoagulant
therapy in addtion to ECS is strongly recommended
Early ambulation without ECS is not recommended due to fear of
dislodging clots and precipititing fatal PE
The practice of having a patient “out of bed into a chair” is one of the
most thrombogenic positions.
Sitting in a chair with the legs in a dependent position causes venous
pooling thromboembolism.
48. Level of Risk Approx DVT Risk
without
Thromboprophylaxis
(%)
Thromboprophylaxi
s option
Very low risk
General or abdominopelvic
surgery
<0.5%
(Rogers
score<7;Caprini score
0)
No specific drugs
Early ambulation
low risk
General or abdominopelvic
surgery
~1.5%
(Rogers score 7-10
Caprini score 1-2)
Mechanical
Prohpylaxis
Moderate risk
General or abdominopelvic
surgery
~3%
(Rogers score>10
7;Caprini score 3-4)
LMWH,LDUH or
mechanial
prophylaxis
High Bleeding risk Mechanical
prophylaxis
High Risk
General or abdominopelvic
surgery
~6%(Rogers
score<7;Caprini score
>5)
LMWH, fondaparinux,
mechanical
prophylaxis
49. References
Schwartz’s Principles of Surgery 10th edition
Sabiston Text book of Surgery 19th Edition
Harrison’s Principle of Internal Medicine 18th
edition
Bailey and Love’s short Practice of Surgery ( 25th)
Washington Manual of Surgery 6th Edition
Medscape