Download to read offline
More Related Content
embolism.ppt
- 1.
- 2. PULMONARY THROMBOEMBOLISM • Fatalform of thromboembolism where occlusion of pulmonary arterial tree occurs by thromboemboli • Pulmonary emboli originates from deep vein thrombosis more commonly • Incidence – 100 – 200 cases/100,000 people in US • Sex –more commonly seen in males than in females
- 3. PULMONARY THROMBOEMBOLISM • Obstructionby thrombosis is uncommon but more commonly by thromboembolism FEATURE PULMONARY THROMBUS PULMONARY THROMBOEMBOLISM Pathogenesis Locally formed Disseminated from thrombus Location In small arteries and branches In major arteries and branches Attachment to vessel wall Firmly adherent Loosely attached or lying freely Gross appearance Head pale, tail red No distinct head and tail, smooth surfaced which is dull and dry Microscopy Platelets and fibrin in layers. Lines of zahn are seen Mixed with blood clot. Lines of zahn are rare
- 4. PULMONARY THROMBOEMBOLISM Risk factors •Stasis of venous blood and hypercoagulable state Causes • Most commonly seen in hospitalized and bed ridden patients • Thrombi originating in large vein of lower legs (deep veins in 95% of thromboemboli) • Less common sources • Thrombus in the varicosities of superficial veins of legs • Pelvic veins such as periprostatic, periovarian, uterine and broad ligament veins
- 5. PULMONARY THROMBOEMBOLISM • Ifthe thrombus is large, it is impacted • at the bifurcation of main pulmonary artery - saddle thrombus • In right ventricle • Its out flow tract
- 6. PULMONARY THROMBOEMBOLISM • Mostlylarge emboli is fragmented into multiple small emboli which are impacted in lower lobes of lungs • Rarely paradoxical embolism occurs – by passage of an embolus from right heart to left heart through atrial or ventricular septal defect
- 7. PULMONARY THROMBOEMBOLISM Consequences ofpulmonary embolism depends upon • Size of occluded vessel • Number of emboli • Cardiovascular status of patient
- 8. PULMONARY THROMBOEMBOLISM CONSEQUENCES OF PULMONARY THROMBOEMBOLISM Suddendeath Due to massive pulmonary embolism or emboli obstructing 60% or more of pulm circulation Acute corpulmonale Numerous small emboli obstruct most of the pulmonary vessels Right heart failure Pulmonary infarct Obstruction of small vessels Pulmonary hemorrhage Obstruction of terminal branches (endarteries) leads to central pulmonary hemorrhage Resolution Pulmonary hypertension Chronic cor pulmonale Pulmonary arteriosclerosis Multiple small emboli undergoing organization rather than resolution Multiple emboli
- 9. AMNIOTIC FLUID EMBOLISM •5th most common cause of maternal mortality world wide • Though incidence is 2 to 6 in 100,000 deliveries death rate is 80% • AFE is rare obstetric complications in which amniotic fluid, hair, fetal cells or other debris enters the maternal circulation leading to cardiorespiratory failure • Process is more similar to anaphylaxis than embolus (anaphylactoid syndrome of pregnancy)
- 10. AMNIOTIC FLUID EMBOLISM Commoncauses of amniotic fluid embolism • Old age • Trauma • Abortion • Caesarian section • Instrumental delivery
- 11. AMNIOTIC FLUID EMBOLISM Pathogenesis •Cause is infusion of amniotic fluid or fetal tissue into maternal circulation via a tear in the placental membranes or rupture of uterine veins
- 12. AMNIOTIC FLUID EMBOLISM •Morbidity and mortality in amniotic fluid embolism is not because of obstruction of pulmonary veins but is due to • Components of amniotic fluid producing anaphylactic reaction • Release of vasoactive substances result from degranulation of mast cells releasing histamine and tryptase • Biochemical activation of coagulation factors, components of complement pathway
- 13. AMNIOTIC FLUID EMBOLISM Amnioticfluid components Amniotic fluid (biochemical mediators) • Surfactant • Endothelin • Leukotriene C4 and D4 • IL – 1 and TNF – α • Thromboxane A2 • Prostaglandins • Arachidonic acid • Thromboplastin • Collagen and Tissue factor III • Phospholipase A2 • PF III Anaphylactic reaction with multisystem involvement Fetal components • Lanugo hair • Vernix caseosa • Fetal squames • Bile stained meconium • Fetal gut mucin • Trophoblasts Mechanical obstruction (minor effects)
- 14. AMNIOTIC FLUID EMBOLISM Progressionoccurs in 2 phases (Cotton1996) Phase I Amniotic fluid and fetal cells in maternal circulation Release of biochemical mediators Pulmonary artery vasospasm Pulmonary hypertension Elevated right ventricular pressure Hypoxia Myocardial and pulmonary capillary damage Left heart failure Acute respiratory distress syndrome
- 15. AMNIOTIC FLUID EMBOLISM PhaseII Biochemical mediators DIC Activation of complement pathway and coagulation factors Hemorrhagic phase Massive hemorrhage and uterine atony
- 16. AMNIOTIC FLUID EMBOLISM Clinicalfeatures • Characterized by severe dyspnea, cyanosis and shock followed by neurologic impairment ranging from headache to seizures, coma and by DIC
- 17. AMNIOTIC FLUID EMBOLISM Findingsat autopsy • Presence of the following substances in pulmonary microvasculature • Squamous cells shed from fetal skin • Lanugo hair • Fat from vernix • Mucin derived from the fetal respiratory or GIT
- 18. FAT EMBOLISM • Refersto presence of microscopic fat globules (sometimes with hematopoietic bone marrow) in the vasculature after the fractures of long bones or rarely in the setting of soft tissue trauma or burns • Injuries rupture sinusoids in the marrow or small veinules allowing marrow or adipose tissue to herniate into the vascular spaces and travel into lung
- 19.
- 20. FAT EMBOLISM Ruptured bloodvessels Fracture in bone
- 21. FAT EMBOLISM Non- traumaticcauses • Agglutination of chylomicrons and VLDL by high levels of plasma CRP • Disease related • Diabetes, acute pancreatitis, burns, SLE and sickle cell crisis • Drug related • Parenteral lipid infusion • Procedure related • Orthopedic surgery, liposuction
- 22. FAT EMBOLISM Fat embolismsyndrome – • Term applied to the minority of patients who become symptomatic • Characterized by • Pulmonary insufficiency • Neurologic symptoms • Anemia • Thrombocytopenia Fatal in 5 – 15% of cases Hypoxemia Neurological abnormalities Petechial rash TRIAD OF FES
- 23. FAT EMBOLISM • Plateletsadhere to fat globules and subsequent aggregation or splenic sequestration - leading to thrombocytopenia • RBCs adhere around fat globules and or subsequent hemolysis – leading to anemia • Rapid onset of thrombocytopenia –leads to petechial rash which is useful diagnostic clue
- 24. FAT EMBOLISM Pathogenesis • Bothmechanical obstruction and biochemical injury Mechanical obstruction – • Fat emboli with associated red cell and platelet aggregates can occlude the pulmonary and cerebral microvasculature Biochemical injury • Release of free fatty acids from fat globules exacerbate the situation by Causing local toxic injury to endothelium and platelet activation and granulocyte recruitment • With release of free radicals, proteases and eicosanoid, more vascular damage occurs
- 25. FAT EMBOLISM 1 to3 days after injury there is sudden onset of • Tachypnea • Dyspnea • Tachycardia • Irritability and restlessness • Further progresses to delirium and coma
- 26. 3 types offat embolism syndrome (Sevitts classification) • Subclinical FES • Non fulminant FES • Fulminant FES
- 27. FAT EMBOLISM Subclinical FES •Occurs around 3 days after trauma • Characterized by decreased PaO2, hemoglobin and platelets • No clinical signs and symptoms of respiratory insufficiency
- 28. FAT EMBOLISM Non fulminantFES • Occurs at any time upto 6 days after trauma • Clinical signs and symptoms are evident • Petechiae, tachycardia, respiratory failure and signs of CNS embolism • Thrombocytopenia, anemia, coagulation abnormalities, • Chest X-ray- pulmonary alveolar and interstitial opacities
- 29.
- 30. FAT EMBOLISM Fulminant FES •Occurs suddenly and rapidly, progressing quickly to death with in few hours of trauma • Clinical features are acute respiratory failure, acute cor pulmonal and neurological embolic changes • These changes result in death of patient shortly after injury
- 31. FAT EMBOLISM • Specialtechniques like frozen section and stains for fat are required to demonstrate fat as lipids dissolve in paraffin embedded sections
- 32. AIR EMBOLISM • Gasbubbles within the circulation can coalesce to form frothy masses that obstruct vascular flow and cause distal ischemic injury • Air embolism occurs when there is communication between the vasculature and outside air and negative pressure gradient “sucks” in air
- 33. AIR EMBOLISM Causes Surgical • Duringneurosurgery in sitting position creating a gravitational gradient and air enters into the cerebral circulation • Introduced during laproscopy and obstetric procedures Non-surgical • During endovascular and interventional procedures • During mechanical ventilation • As a consequence to chest wall injury • Scuba diving, contrast infusion CT scan, CPR
- 34. AIR EMBOLISM • Morethan 100ml is necessary to produce clinical affect in pulmonary vasculature • 300 to 500ml of air at 100ml/sec introduced may be fatal • Emboli trapped in pulmonary vasculature causes • Perfusion blockage of down stream region • Microemboli in capillaries causes intense inflammatory response with release of cytokines that may injure alveoli • Bubbles in CNS may have mental impairment and even sudden onset of coma
- 35. AIR EMBOLISM Venous airentrapment Massive air emboli Entrapment of air in Superior vena cava or Right Atrium or Right Ventricle Impedes flow through heart Decreased cardiac output and decreased blood pressure Small air bubbles
- 36. AIR EMBOLISM Venous airentrapment Massive air emboli Small air bubbles Air lodges in pulmonary capillaries Functional decrease in capillary bed Increased pulmonary arterial pressure and central venous pressure Decreased cardiac output and decreased blood pressure Increased alveolar dead space Decreased PO2 and increased PCO2 Abnormal air blood interface in pulmonary arteries denatures plasma proteins Amorphous proteinaceous and cellular debris created on cell surface Attracts and activates WBC Injury to pulmonary capillary cells and increased permeability Alveolar flooding Non-cardiogenic pulmonary edema
- 37. AIR EMBOLISM Decompression sickness •Occurs when individual experiences sudden decrease in atmospheric pressure • People at risk are • Scuba and deep sea divers • Under water construction workers
- 38. AIR EMBOLISM • Inunderwater partial pressure of nitrogen in breathing air is higher • Nitrogen is not used by body but it gets dissolved in tissues • As the partial pressure increases more and more nitrogen is dissolved in tissues • When the pressure decreases, nitrogen in the tissues comes out
- 39. AIR EMBOLISM Pathogenesis • Ifthe diver ascends too rapidly, nitrogen comes out of solution in the tissues and blood • Rapid formation of gas bubbles with in skeletal muscles and supporting tissues in and about joints is responsible for painful conditions called “the bends” as in 1880 it was noted in those afflicted characteristically arched their backs in a marren reminiscent of then popular womens fashion pose called Grecian bend (photo)
- 40. AIR EMBOLISM • Inthe lungs, gas bubbles in vasculature causes • Oedema • Hemorrhage • Focal atelectasis • emphysema Respiratory distress called chokes
- 41. AIR EMBOLISM Caisson disease •More chronic form of decompression sickness • Named for the pressurized vessels used in bridge construction • Workers in these vessels suffered both acute and chronic form of decompression sickness
- 42. AIR EMBOLISM • Caissondisease • Persistence of gas emboli in skeletal system leads to multiple foci of ischemic necrosis • Common sites – femoral head, tibia and humerus • Treatment – patients are placed in chambers under sufficiently high pressure to force the gas bubbles back into solution • Subsequently slow decompression permits gradual resorption and exhalation of gases which prevents obstructive bubbles from
- 43.