Thromboembolism,pulmonary embolism,general pathology
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ThromboembolismThromboembolism
DR MUHAMMAD ALI BASHIR.
PATHALOGY DEPT.
EMBOLISMEMBOLISM
An embolus is an intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.
The vast majority of emboli derive from a dislodged thrombus—hence the term thromboembolism.
● Emboli
● Thrombosis
● Deep vein thrombosis
Key TermsKey Terms
•Emboli
Clots or other substances that travel through the blood stream and get stuck in a blood vessel, blocking circulation.
• Thrombosis
The development of a blood clot inside a blood vessel.
•Deep vein thrombosis
The development of a blood clot in the calf's deep vein. This frequently leads to pulmonary embolism if untreated.
Most common is pulmonary embolism.Less common types include: fat embolism,air
embolism,amniotic fluid embolism.
•Pulmonary embolism
The occlusion of one or more vessels in the pulmonary arterial tree by matter from a source extrinsic to the lung. The process is almost invariably acuate but may on occasion be chronic.
How dose pulmonary embolism occur ?
Prevalence & Incidence of P.E
● The term 'prevalence' of pulmonary embolism usually refers to the estimated population of people who are managing pulmonary embolism at any given time.
● The term 'incidence’ of pulmonary embolism refers to the annual diagnosis rate, or the number of new cases of pulmonary embolism diagnosed each year.
Incidence (annual): approximately 650,000 cases in the USA
Incidence Rate: approx 1 in 418 or 0.24% in USA
EtiologyEtiology
Pulmonary embolism is caused by emboli that travel through the blood stream to the lungs and block a pulmonary artery. When this occurs, circulation and oxygenation of blood is compromised. The emboli are usually formed from blood clots but are occasionally comprised of air, fat, amniotic fluid, tumor tissue, or particulate matter from intravenous injection, etc.
Common risk factors for pulmonary embolism:
oral contraceptives;the early postpartum period; surgery; DVT; hypercoagulable states; right heart failure;fractures of the pelvic and lower extremities
etc.
congestive heart failure;leukemia; polycythemia; sickle cell anemia; dysproteinemias; massive obesity; immobility; cancer; pregnancy;
any cause of venous stasis
such as: ① venous valvular insufficiency
② right-side HF
③ the postoperative period
④ prolonged bed rest
Risk factors for pulmonary thromboembolism include:
Pathophysiology
Increased pulmonary vascular resistance due to vascular obstruction, neurohumoral agents, or pulmonary artery baroreceptors.
Alveolar hyperventilation due to reflex stimulation of irritant receptors.
Pulmonary embolism can have the following pathophysiological effects:
Decreased pulmonary compliance due to lung edema, lung hemorrhage,and loss of surfactant.
Impaired gas exchange due to increased alveolar dead space from vascular obstruction and hypoxemia, V/Q mismatch.
Increased airway resistance due to broncho- constriction.
SymptomsSymptoms
Each individual may experience symptoms differently, which depend on the size and number of emboli.
● chest pain
● labored breathing, dyspnea, cyanosis
● cough
● syncope
● anxiety
● a rapid pulse.
● a low fever
● hypotension, shock
● fluid build-up in the lungs
DiagnosisDiagnosis
The diagnosis of pulmonary embolism should be based on the patient's history, physical exam, and diagnostic tests.
● Symptoms & Signs
● Plasma D-dimer levels
● ECG
● Arterial Blood Gas
● Chest Radiograph
● Ventilation/Perfusion Lung Scanning
● Pulmonary Angiography
Plasma D-dimer levelsPlasma D-dimer levels
● Low specificity (40-43%) High sensitivity (92-100%)
● Plasma D-dimer levels <500ug/L by ELISA may exclude PE
● S1-Q3-T3
● RBBB (right bundle branch block)
● right axis deviation
● ischemia
● prominent P waves
● tachycardia
● atrial arrhythmia
●Ⅰ0 AVB(atrioventricular block)
ECGECG
S1-Q3-T3
Arterial Blood GasArterial Blood Gas
● hypoxemia ( Po2 )
●respiratory alkalosis ( Pco2 )
● increased A-a(Alveoli-artery) gradient
● can be normal
● pulmonary infiltrate
● pleural effusion
● elevated hemidiaphragm
● atelectasis
● Hampton’s hump ( a pleural-based, wedge-shaped infiltrate )
Chest RadiographChest Radiograph
Posteroanterior chest film of patient with pulmonaryembolism showing "Hampton's hump" in right lower lung field, a homogeneous, wedge-shaped density in the peripheral field, convex to the hilum.
Ventilation Lung Scanning is normal, and perfusion Lung Scanning can show poor flow of blood in areas beyond blocked arteries.
Ventilation/Perfusion Lung ScanningVentilation/Perfusion Lung Scanning
Normal ventilation, perfusion Lung Scanning show poor flow of blood.
The most reliable test for diagnosing pulmonary embolism (“gold standard”)
Pulmonary AngiographyPulmonary Angiography
Right pulmonary arteriogram showedmultiple filling defects clustered mainly around the hilum (arrow)
Pulmonary angiogram with digital subtraction demonstrates a large, acuteembolus in the right lower lobar pulmonary artery (arrowhead).
TreatmentTreatment
Bed rest Haemodynamic and respiratory support Anticoagulation Therapy Thrombolytic Therapy IVC Filter Surgical Therapy
Left, A large embolus in the right pulmonary artery (arrow). Right, After a 2-hour infusion of rt-PA through a peripheral vein, there is pronounced resolution, with only a small amount of residual thrombus in segmental branches.
Inferior vena caval filters. Most filters are placed percutaneouslv via the right femoral vein. Bird's Nest Filter
PrognosisPrognosis
About 10% of patients with pulmonary embolism die suddenly within the first hour of onset of the condition. The outcome for all other patients is generally good; only 3% of patients who are properly diagnosed and treated die. In cases of undiagnosed pulmonary embolism, about 30% of patients die.
PreventionPrevention
Pulmonary embolism risk can be reduced in certain patients through judicious use of antithrombotic drugs such as heparin, venous interruption, gradient elastic stockings and/or intermittent pneumatic compression of the legs.
Fat embolismFat embolism
Soft tissue crush injury or rupture of marrow vascular sinusoids (long bone fracture) releases microscopic fat globules into the circulation.
fat and marrow embolism occurs in some 90% of individuals with severe skeletal injuries but less than 10% show any clinical findings.
The pathogenesis of fat emboli syndrome involves both mechanical obstruction and biochemical injury. Fat microemboli occlude pulmonary and cerebral microvasculature, both directly and by triggering platelet aggregation.
Air embolismAir embolism
Gas bubbles within the circulation can obstruct vascular flow and cause distal ischemic injury.
a small volume of air trapped in a coronary artery during bypass surgery or introduced into the cerebral arterial circulation by neurosurgery performed in an upright “sitting position” can occlude flow, with dire consequences
A particular form of gas embolism called decompression sickness is caused by sudden changes in atmospheric pressure. Thus, scuba divers, underwater construction workers, and persons in unpressurized aircraft who undergo rapid ascent are at risk. When air is breathed at high pressure (e.g., during a deep sea dive), increased amounts of gas (particularly nitrogen) become dissolved in the blood and tissues. If the diver then ascends (depressurizes) too rapidly, the nitrogen expands in the tissues and bubbles out of solution in the blood to form gas emboli, which cause tissue ischemia.
Amniotic fluid embolismAmniotic fluid embolism
The underlying cause is entry of amniotic fluid (and its contents) into the maternal circulation via tears in the placental membranes and/or uterine vein rupture.
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