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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 www.anaesthesia.co.inanaesthesia.co.in@gmail.com
Air enters the vasculature ↓ Pulmonary circulation ↓ Circulatory/Respiratory embarassment
PATHOPHYSIOLOGY Gas in vein ↓ Travels to right heart and lungs ↓ Systemic circulation (If PFO is present)
Entry of air • Abnormal communication between air and blood vessel • Pressure gradient • Trauma • Surgical incision • Intravascular catheters • Mechanical ventilation in patients with damaged lungs
Surgery &Trauma related Non surgical Etiology
Surgical • Neurosurgery • Liver transplant • Total hip replacement • Harrington rod insertion • Spinal fusion • Pulsed saline irrigation • Removal of tissue expanders • TURP • Caesarean section
Arthroscopy • Open heart surgery • Hysterectomy • Head &neck trauma • Dental implant surgery • Pacemaker insertion • IABP • Bone marrow harvest
Epidural catheter placement • Central line removal • Percutaneous lung biopsy • Pulmanary contusion • Laser bronchoscopy • Retrograde pyelography • Haemodialysis • Percutaneous lithotripsy
Non surgical • CPR • GI endoscopy • PPV • Barotrauma • Contrast infusion CT scan • SCUBA diving
Circulatory consequences Massive air embolism ↓ Fills right heart ↓ impedes venous return ↓ stops circulation
>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.
Air passes through right heart to the lungs ↓ raises PA pressure ↓ respiratory consequences
Respiratory consequences Air embolizes in pulmonary arterioles & capillaries ↓ Abnormal air blood interface ↓ Denatures plasma proteins
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
Arterial circulation is protected by filtering effect of pulmonary circulation Large amount of air Lungs can’t filter the air completely.
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
Bronchoconstriction • Hypoxemia • VQ mismatch ↓ ↑ dead space ↓ ↓EtCO2
Extrathoracic manifestations If air directly enters pulmonary veins ↓ Bubbles pass to arterial circulation ↓ Peripheral embolisation ↓ Ischemic manifestations
Brain • Heart • Skin (livedo reticularis)
Some of ischemic manifestations are mediated by PMN WBCs & O2 radicals.
Presentation • Acute hypoxemic respiratory failure • Acute hypoperfusion • Peripheral embolisation
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)
Physical: • Acute respiratory distress • Tachypnea • Tachycardia • Agitation • Disorientation • Classic finding - Mill wheel murmur upon auscultation of the heart • Cyanosis and hypotension - Accompany severe VAE
DIAGNOSIS • Laboratory studies- Hypoxia Hypercapnia Metabolic acidosis
Chest X-Ray- Air in pulmonary arterial system Pulmonary arterial dilatation Focal oligemia (Westermark sign) Pulmonary edema Diffuse alveolar filling
ECG- Tachycardia Right axis deviation Right ventricular strain ST Depression
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.
TEE > Precordial doppler • Identifies RL shunting of air. • Emboli as small as 2µ can be detected. • Signal audiomodulated • 0.5ml Air bubbles heard.
Safety during prolonged use not well established. • Radiofrequency signal of the surgical diarthermy interferes with doppler signal.
EtCO2 ↓es. • Combination of precordial doppler & EtCO2 highly sensitive and specific. • ↑ end tidal & arterial blood CO2gradient. (<0.5) • ↑ed CVP.
Differential Diagnosis • Noncardiogenic pulmonary edema • Cardiogenic pulmonary edema • Volume overload • Sepsis • Gastric acid aspiration
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
Standard Treatment • Mechanical ventilation ↓es work of breathing • Corticosteroids • Anti-inflammatory drugs • Agents against O2 free radicals
Hyperbaric treatment ↓es surface area for activation of WBCs Standard treatment for SCUBA divers
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.
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
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.
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.
FAT EMBOLISM SYNDROME • Fat particles in microcirculation of lungs Lung dysfunction Neurologic manifestations Petechiae
Causes • Traumatic Long bone #s(2-20%) Orthopaedic surgery Blunt trauma to fatty organs Liposuction Bone marrow biopsy
Non Traumatic • Pancreatitis • Diabetes mellitus • Lipid infusions • Sickle cell crisis • Burns • Cardiopulmonary byepass • Decompression sickness • Corticosteroids therapy
Osteomyelitis • Alcoholic fatty liver • Acute fatty liver of pregnancy • Lymphangiography • Cyclosporine infusion
Pathophysiology • Traumatic #boneneutral fat embolisation to pulmonary vasculature hydrolysis of fat ↓ toxic free fatty acids ↓ endothelial injury
Non Traumatic • Hypothesis fat arises from lipids in blood. • ↑CRP - trauma sepsis inflammatory disorders
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.
Systemic Findings • Venous fat emboli across pulmonary circulation ↑ right heart pressures ↓ may open PFO deformable fat emboli enter systemic circulation (fatal)
Clinical Manifestations • 12-72 hrs latent interval • ARDS • Dyspnoea • Hypoxemia • Diffuse lung lesion • Confusion • Obtundation • Coma (cerebral fat embolism)
Petechiae Skin-upper chest,neck and face Retinal vessels – Purtsher’s Retinopathy • Thrombocytopenia • Anemia • Full blown acute right heart syndrome
DIAGNOSIS • Gurd’s Criteria • MAJOR • MINOR • One major & four minor
Diagnosis • Major criteria Petechiae (conjuctiva,axilla)-20-50%cases PaO2 <60 FiO2 >0.4 CNS depression Pulmonary edema Thrombocytopenia >50%↓