1) Pulmonary thromboembolism (PTE) is difficult to diagnose but can be life-threatening, with mortality rates around 30% in haemodynamically unstable patients.
2) PTE is a common cardiovascular emergency caused by emboli blocking pulmonary arteries, and has high morbidity and mortality rates.
3) Autopsy studies have found PTE to be the actual cause of death in up to 15% of hospitalized patients and the leading cause of unexpected in-hospital deaths.
Diagnosis of Pulmonary Embolism is often difficult. This presentation highlights step-wise and practical approach to the diagnosis of PE in short and precise fashion.
Diagnosis of Pulmonary Embolism is often difficult. This presentation highlights step-wise and practical approach to the diagnosis of PE in short and precise fashion.
Physician should have a high suspicion to diagnose patient with pulmonary Embolism, this slides will give you precise Diagnosis, Investigation and guideline directed Treatment.
Pulmonary embolism - Diagnosis and managementDr Vivek Baliga
Pulmonary embolism is a common problem seen in medical practice. This presentation by Dr Vivek Baliga discusses the basic aspects and evidence behind current management.
Physician should have a high suspicion to diagnose patient with pulmonary Embolism, this slides will give you precise Diagnosis, Investigation and guideline directed Treatment.
Pulmonary embolism - Diagnosis and managementDr Vivek Baliga
Pulmonary embolism is a common problem seen in medical practice. This presentation by Dr Vivek Baliga discusses the basic aspects and evidence behind current management.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
2. THE GREAT MASQUERADER
• Pulmonary thrombo embolism(PTE) is important in (ICU) patients where
diagnosis can be difficult and may be life threatening, with mortality rates in
haemodynamically unstable patients being about 30%.
• A relatively common cardiovascular emergency with high morbidity and
mortality.
• Leading cause of unexpected deaths in hospitalized patients. (5-10%)
• Mortality in patients with PE is around 100% in patients with MPE and
hypotension.
• About 90% of patients with fatal PE die within 1-2 hrs of onset.
• Difficult diagnosis that may be missed
• Early diagnosis and aggressive management is the key to successful
outcome.
3. • Average annual incidence of PE is 1:1000 population
in the western countries.
• The exact incidence of PE in India remains
unknown
Wells PS et al. Clin Chest Med 2003.
INCIDENCE
4. • The overall incidence of PE in adult medical autopsies
was 15.9%.
• PE very significantly contributed to death in (80%).
• PE affected a younger population as 80% of the
overall patients (73% were < 50 yrs)
• Sepsis was the primary diagnosis in 32% of total and
in 42% of fatal cases.
N.Kakkar et al. Clinical and Applied Thrombosis/Hemostasis, 2008
An Autopsy-Based Study
(n=1000 adult medical autopsies)
5. • There is 50% resolution of PE after a month of
treatment.
• About 5% of treated pts with PE develop PAH.
• Recurrence rate of PE - 7% at 6 months.
• Mortality rates after an episode of PE are high
with 25 % of patients dying within one year.
Carson JL et al. NEJM 1992
Natural History
8. Risk factors for venous thromboembolism
Primary hypercoagulable states (thrombophilia)
• Antithrombin III deficiency
• Protein C deficiency
• Protein S deficiency
• Resistance to activated protein C (inherited factor
V Leiden mutation)
• Hyperhomocysteinaemia
• Lupus anticoagulant (antiphospholipid antibody)
Secondary hypercoagulable states
• Immobility/Surgery/Trauma/Malignancy
• Pregnancy and the puerperium
• Obesity
• Smoking
• Oestrogen-containing oral contraception or
hormone
• replacement therapy
• Indwelling catheters in great veins and the right
heart
• Burns
• Patients with limb paralysis (e.g. spinal injuries)
• Heart failure
• Increasing age
9. Approximately 20-50% episodes of first-time PE are unprovoked
or idiopathic, that occur without a readily identifiable risk factor.
• Patient-related risk factors (Permanent).
• Setting-related risk factors (Temporary - reversible).
PREDISPOSING RISK FACTORS
13. • Most PE results from DVT of the lower limbs, pelvic veins or inferior vena cava (IVC),
although DVT of the upper limbs, right atrium or ventricle
• Virchow’s triad:
• (1) venous stasis,
• (2) vein wall injury, and
• (3) hypercoagulability of blood does occur.
PATHOPHYSIOLOGY
• Acute pulmonary hypertension increases RV afterload and RV wall tension, which leads to RV dilatation and
dysfunction, with coronary ischaemia being a major contribution
• In massive PE, the combination of coronary ischaemia, RV systolic failure, paradoxical interventricular septal shift
and pericardial constraint leads to left ventricular (LV) dysfunction and obstructive shockting mechanism
• Increased right atrial pressure can open a patent foramen ovale, which may result in right-to-left shunting,
manifested as either refractory hypoxaemia or paradoxical (arterial) embolisation, commonly to the brain,
leading to cerebral infarction
14.
15. Circulatory collapse &
eventually death.
Fall in LV CO and BP
Reduced LV filling during
diastole
RVD & Resultant bulge
of the IVS into the LV
PE - Consequences
RV
RA
LV
LA
16. Precipitates myocardial
ischemia and infarction
Compression & decrease
in perfusion of RCA
Increased RV wall tension
& decrease in Aortic
pressure
PE - Consequences
17. V/Q mismatch
Release of mediators
Hypoxemia
Bronchoconstriction
Lung edema
Lung hemmorhages
Respiratory Failure
PE - Consequences
18. • Massive PE is acute PE characterized by
the presence of hemodynamic instability
(defined by the presence of SBP < 90 mm
Hg).
• Submassive PE is acute PE defined by the
presence of right ventricular dysfunction
but without hemodynamic instability.
(saddle PE)
• Non-massive PE is acute PE without any of
the features of massive or submassive PE.
Definition
19. Classification
• Massive Pulmonary Embolism
• Acute PE with sustained hypotension (SBP 90 mm Hg for at least 15 minutes
or requiring inotropic support,
• Not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or
left ventricular [LV] dysfunction), pulselessness, or
• Persistent profound bradycardia (HR 40 bpm with signs or symptoms of
shock).
• Submassive PE
• Low risk PE
20. Classification
• Massive Pulmonary Embolism
• Submassive PE
• Acute PE without systemic hypotension (SBP> 90 mm Hg) but with either RV dysfunction or
myocardial necrosis
• RV dysfunction means the presence of at least 1 of the following:
• RV dilation
• RV systolic dysfunction
• Elevation of BNP (90 pg/mL) or
• Elevation of N-terminal pro-BNP (500 pg/mL); or
• ECG changes
• new complete or incomplete right bundle-branch block,
• anteroseptal ST elevation or depression, or
• anteroseptal T-wave inversion
• S1Q3T3 pattern
• Myocardial necrosis is defined as either of the following:
• Elevation of troponin I (0.4 ng/mL) or
• Elevation of troponin T (0.1 ng/mL)
• Low risk PE
21. Classification
• Massive Pulmonary Embolism
• Submassive PE
• Low risk PE
• Acute PE and the absence of the clinical markers of adverse prognosis that
define massive or submassive PE.
• 70 to 75% of patients
• Excellent prognosis
23. Symptoms PE confirmed (n - 219) PE excluded (n - 546)
Dyspnoea 80% 59%
Chest pain (pleuritic) 52% 43%
Chest pain (substernal) 12% 8%
Cough 20% 25%
Haemoptysis 11% 7%
Syncope 19% 11%
Signs
Tachypnoea (>20/min) 70% 68%
Tachycardia (>100/min) 26% 23%
Signs of DVT 15% 10%
Fever 7% 17%
Cyanosis 11% 9%
Miniati et al. Resp Crit Care Med 1999, Stein PD et al. Chest 1997
Prevalence of Symptoms & Signs in
Suspected PE
24. Diagnosis-Probability Assessment
• Implicit clinical judgment is fairly accurate: “Do you think this patient
has a PE?”
• Validated prediction rules standardize clinical judgment
• Wells
• Geneva
25. Variables Points
Predisposing factors
Previous PE or DVT 1.5
Immobilization (>3 d) or Surgery in previous 4 wks 1.5
Malignancy 1
Symptoms
Hemoptysis 1
Clinical signs
Heart rate > 100/min 1.5
Clinical signs and symptoms of DVT 3
Clinical judgement
Alternative diagnosis less likely than PE 3
Clinical Probability – Low (0-1), Intermediate (2-6), High (≥ 7)
Well’s Score
26.
27. PERC RULE ( for low risk patients)
• Hormones
• Age > 50yrs
• DVT or PE history
• Coughing up blood(Hemoptysis)
• Lower extremity swelling
• O2 saturation < 95%
• Tachycardia
• Surgery or trauma in past 4 weeks
If none of the 8 PERC features are present in a patient that has deemed low risk by
well’s criteria or by clinical gestalt, then no further tests are indicated.
28. MODIFIED PIOPED CRITERIA FOR DIAGNOSIS
OF PULMONARY EMBOLUS
• Determines the probability of pulmonary embolus following a
V/Q scan.
• Classification
High probability
• 2 or more large mismatched segmental defects or equivalent
moderate /large defects with a normal x ray.
• Any perfusion defect substantially larger than radiographic
abnormality.
29. Intermediate probability
• Multiple perfusion defects with associated radiographic opacities
• > 25 % of a segment and less than 2 mismatched segmental perfusion
defects with
normal radiograph
one moderate segmental
one large or two moderate segmental
one large and one moderate segmental
• Three moderate segmental
• Triple match-solitary moderate – large matching segmental defect with
matching radiograph
• Difficult to characterise high or low probability
30. Low probability
• Non segmental defects ,small effusion, blunting costophrenic angle,
cardiomegaly ,elevated diaphragm, ectatic aorta
• Any perfusion defect with substantialy larger radiographic abnormality
• Matched ventilation and perfusion defects with normal chest
radiograph
• Small subsegmental perfusion defects
• Normal scan
• No perfusion defects
31. DVT
• Non-compressible venous segment
• Increased venous diameter : acute thrombus
• Decreased venous diameter : chronic thrombus
• Loss of phasic flow on Valsalva maneuver
• Absent colour flow : if completely occlusive
• Increased flow in superficial veins
• Lack of flow augmentation of calf squeeze
33. ECG
• sinus tachycardia (which is non-specific), the most frequent ECG
abnormalities
• non-specific S–T depression and T-wave inversion in the anterior leads,
reflecting right heart strain.
• The pattern of a deep S-wave in lead I and a Q-wave and inverted T-wave in
lead III (S1Q3T3) is
• classical, but infrequently present.
• left- or right-axis deviation, P pulmonale, right bundle-branch block and
atrial arrhythmias.
• The ECG is also useful in excluding acute myocardial infarction and
pericarditis.
34.
35. ECG
RV strain - T inversions in V1–V4,
Classic S1Q3T3 type,
Incomplete or complete RBBB
36. CXR
• Focal oligemia (Westermark's sign)
• Peripheral wedged-shaped density above the
diaphragm (Hampton's hump)
• Enlarged right descending PA (Palla's sign).
• Cardiomegaly with pleural effusion
• Atelectasis (loss of lung volume)
• Enlargement of a MPA (Fleischner’s sign)
• Pulmonary parenchymal infiltrate
• Pulmonary congestion
39. Hampton’s hump
Dome shaped pleural based opacity due to lung infarction.
Pulmonary infarct is dome shaped instead of being wedge
shaped because of double blood supply with preserved
bronchial arteries resulting in sparing of the expected apex of
the wedge.
40. 2D ECHO
• the most common being RV dilatation, RV hypokinesis, paradoxical
interventricular septal motion toward the LV, tricuspid regurgitation and
pulmonary hypertension.
• The pattern of RV hypokinesis with apical sparing is considered
pathognomonic for PE.
• The presence of RV dysfunction correlates with mortality.
• a negative echocardiography does not exclude PE.
• TTE: Transthoracic echocardiography will also allow estimation of pulmonary
arterial pressure, identification of intracardiac thrombi (which usually requires
surgical embolectomy) and aids in differential diagnosis by excluding aortic
dissection and pericardial tamponade.
• Transoesophageal echocardiography has the additional benefit of directly
identifying embolus in the proximal pulmonary arteries, which is common in
patients with haemodynamically significant PE.
41.
42.
43.
44. RV dilatation
RV hypokinesia
Dilatation of pulmonary arteries
Moderate to severe TR
Increase in PAP
Paradoxical RV septal motion
Reduced LV cavity dimension &
CO
Right heart thrombi
Thromboemboli in PA (TEE)
Echocardiographic Findings in PE
45. D-dimer
• Sensitivity of >95% and a specificity around 40% (Elisa)
• Normal D-dimer levels excludes acute PE in patients with
either a low or a moderate probability of PE. (High NPV) –
“RULE OUT TEST”
• D-dimer is NOT useful for confirming PE (Low PPV)
• The sensitivity of the D-dimer is > 80% for DVT and >95% for
PE.
Stein PD et al. Ann Intern Med 2004
Based on the new ESC guidelines, instead of a fixed-
cut off level of D-dimers (500 ng/mL), an age-adjusted
cut-off level of D-dimers should be considered to
exclude PE in patients
with low or intermediate clinical possibility for PE and
in those where PE is unlikely
46. Brain Natriuretic Peptides (BNPs)
• Increases in PE
• Reflect the severity of RVD and haemodynamic
compromise
• Elevated levels of BNP or NT-pro-BNP in PE were at
higher risk of
• In-hospital adverse events (OR 6.8, 95% CI 4.4–10)
• 30-day all-cause mortality (OR 7.6, 95% CI 3.4–17)
Klok FA et al. Am J Respir Crit Care Med 2008
47. Cardiac Troponins
• Increases in PE due to RV microinfarction.
• Predict an increase in major complications and
mortality from PE.
• Positive troponin T - 44% in-hospital mortality
Negative troponin T - 3% in-hospital mortality
Gianitsis E et al. Circulation 2000
48. Compression ultrasonography (CUS)
CT Venography
• CUS shows a DVT in 30–50% of pts with PE.
(Sensitivity - 90%, Specificity - 95%)
• The only validated diagnostic criterion for DVT is
incomplete compressibility of the vein.
• CT venography with CT angiography – adds significant
amount of radiation.
49. • Ventilation scans- a gaseous radionuclide xenon or
technetium DTPA in an aerosol form is inhaled
• Perfusion scans - IV injection of radioactive technetium
macro-aggregated albumin (Tc99m-MAA).
• A Gamma Camera acquires the images for both phases
of the study.
• Valid option in dye allergy or renal failure
V/Q Scan
50. Scintigraphy
(ventilation perfusion lung scan)
Advantages:
Very high sensitivity 98% (it was the imaging modality of choice in
diagnosis of pulmonary embolism).
Disadvantages:
The main one was high percentage of non diagnostic intermediate
probability scans.
Very low specificity 10%.
52. V/Q Scan Interpretation
RESULT INTERPRETATION SIGNIFICANCE
Normal No Perfusion Deficit Excludes PE
Low
Probability
Perfusion Deficit with
matched Ventilation Deficit
Non Diagnostic
Intermediate
Probability
Perfusion Deficit that
corresponds to
Parenchymal Abnormality
on CXR
Non Diagnostic
High
Probability
Multiple Segmental
Perfusion Deficits with
Normal Ventilation
Diagnostic for PE
53. • Sensitivity and specificity: 41% and 97%
• Normal perfusion scan excludes PE.
• High-probability V/Q scan Confirms PE.
• May need further tests to exclude PE, if negative in pts
with high clinical probability. (low PPV)
• May NOT be reliable for the diagnosis of PE in the
presence of pre-existing pulmonary disease (pleural
effusion, COPD)
• Lower radiation exposure than Spiral CT
PIOPED II study, 2008
V/Q Scan Interpretation
54. • Imaging test of choice for the diagnosis of PE
• Sensitivity of 83% and Specificity of 96%
• Positive MDCT confirms PE
• A negative MDCT excludes PE in patients with a
non-high clinical probability of PE (NPV 90%)
• A negative MDCT despite a high clinical
probability – Further tests required. (NPV 60%)
PIOPED II study, 2008
MDCT Pulmonary Angiography
The PIOPED II trial observed a sensitivity of 83% and a
specificity of 96% for MDCT
65. • MR utilizes gadolinium contrast agent, which is not
nephrotoxic.
• MR imaging should be considered for suspected PE
with renal insufficiency or contrast dye allergy.
• MR pulmonary angiography detects large proximal PE
but is not reliable for smaller segmental and
subsegmental PE.
MR (Contrast Enhanced)
Pulmonary Angiography
66. Pulmonary MRA
• Pulmonary hypertension with dilated central pulmonary arteries and
pruning of peripheral pulmonary arteries
67.
68. Pulmonary Angiography
• Now rarely employed
• Performed when the results of non-invasive imaging
are equivocal.
• Mortality due to pulmonary angiography -0.2%
• Risk of local bleeding is markedly increased due to
thrombolysis after pulmonary angiography.
Agnell D et al. Arch Intern Med 2002
69. Pulmonary angiographic findings
Primary signs:
The only primary sign of acute pulmonary embolism is filling defect.
Secondary signs:
Abrupt occlusion of pulmonary artery.
Areas of oligemia with pruning of the branching vessels.
73. HISTORICAL ASPECTS
Peitho trial
Fibrinolysis for patients with intermediate risk
Conclusion – In patients with intermediate risk pulmonary embolism,
fibrinolytic therapy prevented hemodynamic decompensation but
increased the risk of major hemorrhage and stroke
Moppet trial
Moderate pulmonary embolism treated with thrombolysis
Conclusion-low dose thrombolysis is safe and effective in moderate
PE
74. Mappet trial 1
Management strategies and determinants of outcome in acute major
pulmonary embolism -multicentre registry 1997
Conclusion- Thrombolysis may favorably affect the clinical outcome of
hemodynamically stable patients with major pulmonary embolism.
Mappet trial 2
Importance of cardiac troponins I and T in risk stratification of
patients with acute pulmonary embolism
Conclusion-CTni and CTnT may be a novel , particularly useful tool for
optimizing the management strategy in patients with acute PE.
Mappet trial 3
Management strategies and prognosis of pulmonary embolism
Heparin plus alteplase compared with heparin alone in patients with
Sub massive PE.
Conclusion – alteplase may improve clinical course and prevent further
clinical or hemodynamic deterioration.
75. Pioped 1 study
Provide a comprehensive criteria for v/q lung scan interpretation
Conclusion -study support the use of v/q lung scanning in the diagnostic
evaluation of patients with suspected reammendments to the original pioped
criteria should reinforce the role of v/q lung scanning in patients with suspected
PE
Pioped 2 study
The accuracy of multidetector CTA for the diagnosis of acute PE.
Conclusion-In pts with suspected PE multidetector cta-ctv has a higher
diagnostic sensitivity than does cta alone. with similar specificity. The predictive
value of either cta-ctv is high with concordant clinical assessment but additional
testing is necessary when the clinical probability is inconsistent with imaging
results.
Pioped 3 study
Gadolinium enhanced mra for PE
Conclusion mrpa should only be considered at centres that routinely perform it
well and only for patients for whom standard tests are contraindicated.
87. • Respiratory support
• Inotropic support
• IV Fluids
• Anticoagulation
• Thrombolysis
• Embolectomy (Surgical /
Percutaneous catheter)
Primary
Therapy
TREATMENT
88. IV UFH
(bolus 80 U/kg followed by infusion at 18 U/kg/h)
S/C LMWH
Enoxaparin (1mg/kg BD), Tinzaparin, Dalteparin
S/C Fondaparinux
5 mg (<50 kg) 7.5 mg (50-100 kg), 10 mg (>100 kg) OD
Anticoagulation
89. Anticoagulation
IV UFH is the preferred
anticoagulant of choice:
1. Hypotension
2. Severe renal failure
3. High risk bleeding
92. Loading
dose
2.5 million IU
over 30 mins
Maintenance
dose
1 million IU/hr
over 12-24 hrs.
Accelerated
regimen
1.5 million IU
over 2 hrs
THROMBOLYSIS
Streptokinase
93. Loading
dose
4400 IU/kg
over 10 mins,
Maintenance
dose
4400 IU/kg/hr
over 12-24 hrs.
Accelerated
regimen
3 million IU over 2
hrs
THROMBOLYSIS
Urokinase
94. 100mg
over 2 hrs
Accelerated Regimen Over 1.5 hrs
15mg bolus
0.75mg/kg (50mg) over 30mins
0.5 mg/kg (35mg) over 60 mins
THROMBOLYSIS
rtPA
95. Reteplase
(Two IV boluses of 10 U each 30 mins
apart)
Tenecteplase
0.5mg/kg (30-50mg) bolus over 5 secs
THROMBOLYSIS
96. • Prior intracranial hemorrhage (ICH)
• Cerebral vascular lesion / neoplasms
• Ischemic stroke in preceding 6 months
• Active bleeding or bleeding diathesis (excluding
menses)
• Recent major trauma / surgery / head injury within 3
wks
Contraindications of Thrombolysis in PE
(Absolute)
97. • Uncontrolled HTN (SBP >180 mm Hg or DBP >110
mm Hg)
• Traumatic resuscitation
• Recent (within 2-4 wk) internal bleeding
• Noncompressible vascular punctures
• Pregnancy or within 1 week of postpartum
• Active peptic ulcer
• Oral anticoagulant therapy with (INR) >1.7 or PT
>15 seconds
Contraindications of Thrombolysis in PE
(Relative)
98.
99. NEW ORAL ANTICOAGULANTS: (nVk antagonists)
• Various studies on non – vitamin K – dependent new oral anticoagulants show
following results:
• 1. In RECOVER trial – the direct thrombin inhibitor Dabigatran (150 mg BD)
was compared with warfarin for the treatment of VTE – with regard to efficacy
Dabigatran was non – inferior to warfarin.
• 2. In EINSTEIN-PE trial – single oral drug treatment with direct factor Xa
inhibitor Rivaroxaban (15 mg twice daily for 3 weeks, followed by 20 mg once
daily) was tested against Enoxaparin / warfarin & was found to be non –
inferior.
100. 3. The AMPLIFY study – compared single oral drug treatment using direct factor Xa
inhibitor Apixaban (10 mg twice daily for 10 days, followed by 5 mg once daily) with
conventional therapy (Enoxaparin / Warfarin)
• The primary efficacy outcome was recurrent symptomatic VTE or death related to
VTE.
• Apixaban was non – inferior to conventional therapy for the primary efficacy
outcome.
4. The Hokusal-VTE study – compared the direct factor Xa inhibitor Edoxaban (60
mg OD, reduced to 30 mg OD if CrCL is 30 – 50 ml/min or body weight is < 60 kg)
with conventional therapy (UFH or Enoxaparin/Warfarin)
• Edoxaban was non – inferior to warfarin with respect to primary efficacy outcome
of recurrent symptomatic VTE or fatal PE.
101.
102. Valuable Therapeutic Option in pts with:
1. Failed thrombolysis
2. Contraindication to thrombolysis
EMBOLECTOMY
(Surgical / Percutaneous catheter)
103. SURGICAL EMBOLECTOMY:
• The merit of surgical pulmonary embolectomy for pts with
massive PE, is questionable since the advent of
thrombolytic therapy.
• It is associated with peri-operative mortality of 25 – 50%.
• It is indicated in pts with PE & hypotension who have
absolute contraindications to thrombolytic therapy or if
thrombolytic therapy has failed.
• It may also be useful when pts have free – floating intra-
cardiac thrombus.
104. PERCUTANEOUS EMBOLECTOMY: include either
• embolus extraction techniques (pure percutaneous
embolectomy) or
• embolus destruction technique ( including catheter-
directed thrombolytic therapy & percutaneous thrombus
fragmentation technique)
• Success rates are over 80% with reasonable
complications.
• Should be considered in pts with contra-indications to
systemic thrombolytic therapy who are in specialised
centers.
106. • INFERIOR VENACAVA FILTERS: (IVC – Filters)
• This is another method to prevent further embolisation.
• Placed in the infra – renal portion of IVC.
• If thrombus is identified in renal veins, supra – renal
placement may be indicated.
• Absolute indications are:
• - absolute contra-indications to anti-coagulants
• - new or recurrent PE despite anti-coagulation
• - complications resulting from anti-coagulation.
• Other recommended indications include:
• - pts with extensive DVT
• - following surgical embolectomy
• - following thrombolytic therapy.
107. • Early complications:
• - insertion site thrombosis (10% of pts)
• - placement in SVC, carries risk of pericardial tamponade
• Late complications:
• - recurrent DVT (20% of pts)
• - post thrombotic syndrome (in up to 40% pts)
• - occlusion of IVC in 22% pts at 5 years.
• 8 yr follow-up of a randomized study on 400 pts with DVT (with
or without PE) who had received anticoagulant for initial 3
months showed – pts with permanent IVC filters had reduced
risk of recurrent PE – at the cost of increased risk of recurrent
DVT – no overall effect on survival.
108. • Non – permanent IVC filters are classified as temporary or
retrievable devices.
• Temporary filters must be removed within few days.
• Retrievable filters can be left in place for longer periods.
• Non – permanent filters should be removed as soon as it is
safe to use anticoagulants.
• If left in situ for longer periods – late complications like filter
migration, tilting or deformation, penetration of the caval wall
by filter limbs, fracturing of the filter & embolisation of the
device occurs.
• There is no evidence to support the use of IVC filters in pts
with free-floating thrombi in proximal veins & in pts posted for
thrombolysis, surgical embolectomy or pulmonary
thrombendarterectomy.
109. Long Term Anticoagulation
• Initiation of vitamin K antagonists (Warfarin) is
recommended on the first treatment day. (INR
target: 2.0-3.0) (Grade 1A)
• Duration of oral anticoagulation (3 mths for
secondary PE, > 3 mths for idiopathic PE)
• Recurrence of unprovoked PE - indefinite
treatment is recommended.
• Dabigatran, Rivaroxaban, Apixaban - currently
under phase III trials.
Kearon C et al. JAMA 2006
110. Duration of anticoagulation
• Patients with PE should receive at least
3 months of anticoagulant treatment
• The risk of recurrence if anticoagulants
are stopped after 6 or 12 months can
expected to be similar to that after 3
months
• Indefinite treatment reduces the risk for
recurrent VTE by about 90%, but this
benefit is partially offset by a 1% or
higher annual risk of major bleeding.
• Patients with cancer are candidates for
indefinite anticoagulant treatment
after an initial episode of PE
• For cancer patients LMWH for 6 months
after that it could be either LMWH or
VKA till the disease is active
111. Duration of Anticoagulation
• For patients with provoked PE, treatment with a VKA for 3 months is
preferable
• Unprovoked PE should be treated with VKA for at least 3 months.
After this period, indefinite anticoagulation therapy should be
considered for patients with a first unprovoked proximal DVT or PE
and a low risk of bleeding
• Lifelong treatment is recommended for most patients with a second
unprovoked DVT or PE
113. CONCURRENT HAEMODYNAMIC SUPPORT:
• Shocked pts with PE (massive PE) need urgent
• haemodynamic support in addition to attempts at
• embolus destruction and
• prevention of further embolisation.
• 1) IV FLUIDS:
• Volume loading can improve haemodynamic status in pts with massive PE
• But excessive fluid therapy may worsen RV function (by mechanical
overstretch), which in turn affects LV function.
• There fore modest fluid challenges (500ml) may help to increase cardiac index
114. • 2) VASOPRESSORS:
• Use of vasopressors is often necessary, in parallel with
pharmacological, surgical or interventional reperfusion.
• Nor epinephrine appears to improve RV function via direct
positive inotropic effect, while also improving RV coronary
perfusion by stimulation of peripheral vascular α-receptors
there by increasing MAP.
• RVCPP = MAP – RVPm
• RVCPP – RV coronary perfusion pressure.
• MAP – mean arterial pressure
• RVPm – mean RV pressure
• RVPm = CVP + 1/3 (PAPs – CVP)
• CVP – central venous pressure
• PAPs – systolic pulmonary arterial pressure.
115. • Dopamine & Dobutamine may be considered for pts of
PE with low cardiac index.
• However raising cardiac index above physiological values
may aggravate ventilation – perfusion mismatch by
redistributing flow from obstructed to non-obstructed
vessels.
• Vasodilators decrease pulmonary arterial pressure &
pulmonary vascular resistance, but may be harmful due
to lack of specificity – cause systemic vasodilatation & fall
in MAP.
• There fore Isoprenaline, Nitroglycerine, Nitroprusside &
Dobutamine or Milrinone should be considered only if
MAP is adequate.
116. • SELECTIVE PULMONARY VASODILATORS:
• Inhaled nitric oxide may improve haemodynamic status &
gas exchange of severely hypoxemic PE pts.
• Inhaled prostacyclin is an alternative.
• OTHER MANAGEMENT ISSUES:
• Hypoxaemia and hypocapnia (due to dead space
ventilation & hyperventilation) require high flow oxygen.
• Intubation & mechanical ventilation often necessary in pts
with massive PE.
• Care should be taken to limit positive intrathoracic
pressure by applying PEEP with caution – as it may
reduce venous return & worsen RV failure in pts with
massive PE.
117. • Low tidal volumes (approximately 6 ml/kg lean body
weight) should be used to keep end-inspiratory plateau
pressure ˂ 30 cm H2O.
• To guide resuscitation central venous catheter (before
administering thrombolytic therapy) should be secured.
• Extracorporeal membrane oxygenation (ECMO) should
be considered for pts with PE who have had
cardiopulmonary arrest or have very severe shock.
118.
119. AHA PE GUIDELINES
• Anticoagulation with LMWH ,UFH or fondaparinux. –I/A
• While working up PE, if pretest is moderate or high and there are no
contraindications, start anticoagulation during work up. –I/C
• Fibrinolysis is reasonable for patients with massive PE and acceptable risk
of bleeding complications.-II a/B
• Fibrinolysis may be considered for patients with submassive PE; judged to
have clinical evidence of adverse prognosis and low risk of bleeding
complications – II b/C
• Fibrinolysis is not recommended for patients with submassive PE with only
mild dysfunction – III/B
• Fibrinolysis is not recommended for undifferentiated cardiac arrest – III/B
120. • Either catheter embolectomy or surgical
embolectomy can be considered depending on
institutional and operator preference- IIa/C
• Either of interventional or surgical options are
reasonable if the patient is still unstable in massive PE
after fibrinolysis- IIa/C
• Also reasonable in massive PE , if the patient has a
contraindication to lysis-IIa/C
• May be considered in lieu of fibrinolysis in patients of
submassive PE and evidence of adverse prognosis-
IIb/C
• Not recommended for patients with PE at low risk-
III/C
121. • Pulmonary embolism in pregnancy:
• Risk of VTE increases during pregnancy and during post partum period, PE is the
leading cause of death.
• DVT and PE are common during all trimester of pregnancy and 6- 12 week after
delivery.
• Diagnosis:
• The diagnostic approach to patient with PE is same as non pregnant women
nuclear perfusion scan is in pregnancy as is a chest CT scan.
• Treatment:
• Heparin(LMWH) and fibrinolysis are safe in pregnancy.
• Warfarin is contraindicated because it crosses placenta and causes fetal
malformation.
• Unfraction heparin is category C drug.
• Women experiencing TE event during pregnancy a full dose of LMWH can be
start and continue till pregnancy and 4-6 weeks postpartum.
125. Supportive Care:
• Compression and stockings:
• For a patients who had a proximal DVT, the use of elastic compression
stocking provides a safe and effective adjunctive treatment that can limit
post phebilitic syndrome
• Socking with a pressure of 30-40mmhg at the ankle reduces the risk of post
phlebitic syndrome.
• True gradient compression stockings are highly elastic and provide a
compression gradient more at ankle and gradually reduces till thigh, this
reduces capacitive venous volume by approx 70% and increase velocity of
blood flow in deep vein which are effective in prophylaxis of thrombo
embolism and prevent prognosis of thrombus in patient with DVT and PE.
• In pregnant women stockings of pressure 30 -40mm hg are use to prevent
DVT and prevent development of varicose vein.
Editor's Notes
The overall incidence of PE in adult medical autopsies was 15.9 percent and was a terminal event in almost 80 percent of these patients
perfusion eventually returns to normal in 2/3 of patients
because of poor resolution of the thromboemboli.
Despite anticoagulant therapy, VTE recurs frequently in the first few months after the initial event, with a rate of 7% in 6 mths.
Immediate bedside clinical assessment for the presence or
absence of clinical markers allows stratification into high-risk and
non-high-risk PE
High-risk PE is a life-threatening emergency requiring specific
diagnostic and therapeutic strategy (short-term mortality
.15%).17,51
Non-high-risk PE can be further stratified according to the
presence of markers of RVD and/or myocardial injury into
intermediate- and low-risk PE. Intermediate-risk PE is diagnosed if at
least one RVD or one myocardial injury marker is positive. Low-risk
PE is diagnosed when all checked RVD and myocardial injury
markers are found negative
In 90% of cases, suspicion of PE is raised by clinical symptoms like dyspnea, tachypnea, tachycardia, syncope. U can see here in this series of dyspnea, tachypnea, tachycardia were seen more commonly.
Individual clinical signs and symptoms are not very helpful, as they are neither sensitive nor specific
The above changes in ECG may be helpful in some cases, particularly of new onset.
Although D-dimer is very specific for fibrin, the specificity of fibrin for VTE is poor because fibrin is produced
in a wide variety of conditions, such as cancer, inflammation, infection, necrosis, dissection of the aorta, and the positive predictive value (PPV) of D-dimer is low. Therefore, D-dimer is not useful for confirming PE. The D-dimer assay is not specific. Levels increase in patients with myocardial infarction, pneumonia, sepsis, cancer, the postoperative state and second or third trimester of pregnancy
CUS shows a DVT in 30–50% of patients with PE, and finding a proximal DVT in patients suspected of PE is sufficient to warrant anticoagulant treatment without further testing
V/Q scan is a well established and robust diagnostic test for PE, especially in dye allergy and renal failure. Ventilations scans are combined with perfusion scans.
Unfortunately, most patients have nondiagnostic scans, and fewer than half of patients with angiographically confirmed PE have a high-probability scan.
SDCT or MDCT showing a thrombus up to the segmental level can be taken as adequate evidence of PE. A negative SDCT must be combined with negative CUS to safely exclude PE, whereas MDCT may be
used as a stand-alone test.
Subcutaneous fondaparinux was
associated with a similar rate of recurrent VTE (3.8% versus
5.0% (UFH group) at 3 months; absolute difference -1.2%, 95%
CI -3.0–0.5%), major bleeding (1.2% versus 1.1% (UFH) at the
end of initial treatment) and rate of death (5.2% versus 4.4%
(UFH) at 3 months) as compared with adjusted intravenous
UFH [63].
The determination of optimal duration of anticoagulant
treatment represents a balance between the estimated risk of
recurrence after treatment discontinuation and the risk of
bleeding complications under treatment. However, the rate of fatal PE remains low after the
cessation of anticoagulant treatment and does not appear to be
higher than the risk of fatal bleeding during prolonged
anticoagulant treatment [76, 77]. In randomised controlled
trials, the rate of recurrent VTE is generally higher in patients
receiving short-term treatment of 6 weeks to 6 months than in
patients given more prolonged treatment [72, 73, 78]. However,
in most studies, the patients were not followed after treatment
cessation and the number of patients with PE included was
generally small. It remains unclear whether prolonged anticoagulant
treatment reduces the long-term rate of recurrent VTE
or simply delays subsequent VTE events. According to the
eighth edition of the American College of Chest Physicians
guidelines, patients with PE secondary to a transient risk factor
should be treated for 3 months and those with idiopathic PE
should be treated for >3 months