thromboembolism,pulmonary embolism,general pathology

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.