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AIR EMBOLISM SYNDROME

AIR EMBOLISM SYNDROME. www.anaesthesia.co.in anaesthesia.co.in@gmail.com. Air enters the vasculature ↓ Pulmonary circulation ↓ Circulatory/Respiratory embarassment. PATHOPHYSIOLOGY. Gas in vein ↓ Travels to right heart and lungs ↓

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AIR EMBOLISM SYNDROME

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  1. AIR EMBOLISM SYNDROME www.anaesthesia.co.inanaesthesia.co.in@gmail.com

  2. Air enters the vasculature ↓ Pulmonary circulation ↓ Circulatory/Respiratory embarassment

  3. PATHOPHYSIOLOGY Gas in vein ↓ Travels to right heart and lungs ↓ Systemic circulation (If PFO is present)

  4. Entry of air • Abnormal communication between air and blood vessel • Pressure gradient • Trauma • Surgical incision • Intravascular catheters • Mechanical ventilation in patients with damaged lungs

  5. Surgery &Trauma related Non surgical Etiology

  6. Surgical • Neurosurgery • Liver transplant • Total hip replacement • Harrington rod insertion • Spinal fusion • Pulsed saline irrigation • Removal of tissue expanders • TURP • Caesarean section

  7. Arthroscopy • Open heart surgery • Hysterectomy • Head &neck trauma • Dental implant surgery • Pacemaker insertion • IABP • Bone marrow harvest

  8. Epidural catheter placement • Central line removal • Percutaneous lung biopsy • Pulmanary contusion • Laser bronchoscopy • Retrograde pyelography • Haemodialysis • Percutaneous lithotripsy

  9. Non surgical • CPR • GI endoscopy • PPV • Barotrauma • Contrast infusion CT scan • SCUBA diving

  10. Circulatory consequences Massive air embolism ↓ Fills right heart ↓ impedes venous return ↓ stops circulation

  11. >100 ml of air must be acutely infused to arrest circulation. • In animal experiments,rate of venous air infusion .03ml/kg/mt • In an 70 kg adult,@21ml/mt.

  12. Air passes through right heart to the lungs ↓ raises PA pressure ↓ respiratory consequences

  13. Respiratory consequences Air embolizes in pulmonary arterioles & capillaries ↓ Abnormal air blood interface ↓ Denatures plasma proteins

  14. Amorphous proteinaceous & cellular debris created at the surface of air bubbles ↓ Attracts and activates WBCs ↓ Injury to pulmonary capillaries ↓ ↑ capillary permeability ↓ Alveolar flooding ↓ Non cardiogenic pulmonary edema

  15. Arterial circulation is protected by filtering effect of pulmonary circulation Large amount of air Lungs can’t filter the air completely.

  16. Right heart  bubbles can pass to left side Pressure left side>right side Significant pulmonary embolisation ↑es right heart pressure ↓ Reversal of interatrial gradient ↓ Systemic embolisation

  17. Bronchoconstriction • Hypoxemia • VQ mismatch ↓ ↑ dead space ↓ ↓EtCO2

  18. Extrathoracic manifestations If air directly enters pulmonary veins ↓ Bubbles pass to arterial circulation ↓ Peripheral embolisation ↓ Ischemic manifestations

  19. Brain • Heart • Skin (livedo reticularis)

  20. Some of ischemic manifestations are mediated by PMN WBCs & O2 radicals.

  21. Presentation • Acute hypoxemic respiratory failure • Acute hypoperfusion • Peripheral embolisation

  22. Symptoms, which develop immediately following embolization, are similar to pulmonary thromboembolism. Severity of symptoms is related to degree of air entry and include the following: • Dyspnea • Chest pain • Tachycardia • Hypotension • Altered sensorium • Circulatory shock or sudden death (patients with severe VAE)

  23. Physical: • Acute respiratory distress • Tachypnea • Tachycardia • Agitation • Disorientation • Classic finding - Mill wheel murmur upon auscultation of the heart • Cyanosis and hypotension - Accompany severe VAE

  24. DIAGNOSIS • Laboratory studies- Hypoxia Hypercapnia Metabolic acidosis

  25. Chest X-Ray- Air in pulmonary arterial system Pulmonary arterial dilatation Focal oligemia (Westermark sign) Pulmonary edema Diffuse alveolar filling

  26. ECG- Tachycardia Right axis deviation Right ventricular strain ST Depression

  27. Transthoracic/transesophageal Echocardiography- Air in right ventricular outflow tract/major pulmonary veins • Precordial Doppler Right or left 2nd to 4th intercostal space in parasternal location.

  28. TEE > Precordial doppler • Identifies RL shunting of air. • Emboli as small as 2µ can be detected. • Signal audiomodulated • 0.5ml Air bubbles heard.

  29. Safety during prolonged use not well established. • Radiofrequency signal of the surgical diarthermy interferes with doppler signal.

  30. EtCO2 ↓es. • Combination of precordial doppler & EtCO2 highly sensitive and specific. • ↑ end tidal & arterial blood CO2gradient. (<0.5) • ↑ed CVP.

  31. Differential Diagnosis • Noncardiogenic pulmonary edema • Cardiogenic pulmonary edema • Volume overload • Sepsis • Gastric acid aspiration

  32. Management • Prevent reembolisation • Support respiration & circulation • Identify & close source of air entry. • ↓ gradient Notify surgeon Flood operating field with saline FiO2 1 Pressors & ionotropes Jugular compression • Retrieve air

  33. Standard Treatment • Mechanical ventilation ↓es work of breathing • Corticosteroids • Anti-inflammatory drugs • Agents against O2 free radicals

  34. Hyperbaric treatment ↓es surface area for activation of WBCs Standard treatment for SCUBA divers

  35. Emergency Department Care: • Once VAE is suspected, any central line procedure in progress is immediately terminated and the line is clamped. • Do not withdraw the catheter at this time unless it cannot be clamped.

  36. Promptly place patient in Trendelenburg position and rotate toward the left lateral decubitus position. This maneuver helps trap air in the apex of the ventricle, prevents its ejection into the pulmonary arterial system, and maintains right ventricular output. • Administer 100% oxygen and intubate for significant respiratory distress or refractory hypoxemia

  37. If CV catheter is present, aspirate from the distal port and attempt to remove air. Catheter may have to be advanced for this to be successful. • In circulatory collapse, external cardiac compression may help expel air from the pulmonary outflow tract and disperse it into the peripheral pulmonary venous system. Support right ventricular function with fluid administration and beta-adrenergic agents, if indicated.

  38. Experience with hyperbaric oxygen therapy for VAE is limited, but experience suggests significant efficacy. If this modality is available, arrange transportation to a hyperbaric facility without delay.

  39. FAT EMBOLISM SYNDROME • Fat particles in microcirculation of lungs Lung dysfunction Neurologic manifestations Petechiae

  40. Causes • Traumatic Long bone #s(2-20%) Orthopaedic surgery Blunt trauma to fatty organs Liposuction Bone marrow biopsy

  41. Non Traumatic • Pancreatitis • Diabetes mellitus • Lipid infusions • Sickle cell crisis • Burns • Cardiopulmonary byepass • Decompression sickness • Corticosteroids therapy

  42. Osteomyelitis • Alcoholic fatty liver • Acute fatty liver of pregnancy • Lymphangiography • Cyclosporine infusion

  43. Pathophysiology • Traumatic #boneneutral fat embolisation to pulmonary vasculature hydrolysis of fat ↓ toxic free fatty acids ↓ endothelial injury

  44. Non Traumatic • Hypothesis fat arises from lipids in blood. • ↑CRP - trauma sepsis inflammatory disorders

  45. serum of acutely ill patients has the capacity to agglutinate chylomicrons , VLDL & liposomes of nutritional fat emulsions -CRP provokes Ca dependent agglutination of each of these lipid containing substances.

  46. Systemic Findings • Venous fat emboli across pulmonary circulation ↑ right heart pressures ↓ may open PFO deformable fat emboli enter systemic circulation (fatal)

  47. Clinical Manifestations • 12-72 hrs latent interval • ARDS • Dyspnoea • Hypoxemia • Diffuse lung lesion • Confusion • Obtundation • Coma (cerebral fat embolism)

  48. Petechiae Skin-upper chest,neck and face Retinal vessels – Purtsher’s Retinopathy • Thrombocytopenia • Anemia • Full blown acute right heart syndrome

  49. DIAGNOSIS • Gurd’s Criteria • MAJOR • MINOR • One major & four minor

  50. Diagnosis • Major criteria Petechiae (conjuctiva,axilla)-20-50%cases PaO2 <60 FiO2 >0.4 CNS depression Pulmonary edema Thrombocytopenia >50%↓

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