Air embolism

anaesthesia

1. AIR EMBOLISM An  embolism  is the lodging of an  embolus, a blockage-causing piece of material, inside a blood vessel .  The embolus may be a blood clot ( thrombus ) , a fat globule (fat embolism), a bubble of air or other gas (gas embolism), or foreign material. An embolism can cause partial or total blockage of blood flow in the affected vessel .  Such a blockage (a vascular occlusion) may affect a part of the body distant to the origin of the embolus. An embolism in which the embolus is a piece of thrombus is called a thromboembolism.

2. Air embolism Any gas can result in embolization if present in vasculature. So air embolism can be : Venous air embolism Arterial air embolism Paradoxical air embolism i.e venous embolism can cross to systemic circulation via congenital defect like patent foramen ovale .

3. Risk factors for Air Embolism

4. Clinical manifestation A volume of 5ml/kg is considered large enough to cause cardiovascular collapse due to reduction in cardiac output. Some of the clinical manifestation which can be seen are as follows: Chest pain Arrythmia Right ventricular failure Cardiac arrest Sudden drop in EtCO2 due to dead space ventilation Hypercarbia, hypoxaemia due V/Q mismatch

5. Acute lung injury due to triggering of inflammatory response. Shortness of breath Haemoptysis can be a late sign Ischaemic stroke which can be clinically manifested as failure to wake up following general anaesthesia. May cause seizure, confusion in awake patient.

6. Veneous Air Embolism Venous air emblism can occur whenever the operative site is higher than Right Atrium. Incidence is more in some neurosurgeries like craniotomy in sitting position, posterior fossa surgeries. A large volume of air within right atrium may cause frothing resulting in right atrium outflow obstruction which causes decrease in cardiac output. Significant embolism can lead to : Hypotension tachycardia Altered mental status, decreased councious level

7. Auscultation of heart might reveal mill wheal murmur. Pulmonary edema may develop in later stage. End tidal carbon dioxide level falls due to increase in physiological dead space. ABG might reveal hypoxemia and hypercarbia . Chest x ray can show signs of non-cardiogenic pulmonary edema. Hypoxia may develop along with the reflex sympathetic vasoconstriction of vessels.

8. In the case of massive VAE the generation of an air lock may occur. This air lock is essentially a complete outflow obstruction leading to no forward blood flow, an increased wall tension in the right ventricle (RV ),an increased myocardial oxygen consumption of the RV, RV ischemia, and ultimately cardiovascular collapse .

9. More modest volumes may still result in significant right ventricular outflow obstruction that can also trigger the humoral agents’ release of inflammatory mediators, bronchoconstriction, increase in ventilation/perfusion mismatch, and reflex vasoconstriction previously mentioned . Differential diagnosis like pulmonary embolism, pneumothorax must be taken into consideration.

10. DETECTION OF VENOUS AIR EMBOLISM The monitors used for the detection of VAE should provide (1 ) a high level of sensitivity ( 2) a high level of specificity ( 3) a rapid response (4 ) a quantitative measure of the VAE event, and ( 5) an indication of the course of recovery from the VAE event.

11. The combination of a precordial Doppler and expired CO2 monitoring meets these criteria and is the current standard of care. Doppler placement in a left or right parasternal location between the second and third or third and fourth ribs has a very high detection rate for gas embolization and when good heart tones are heard, maneuvers to confirm adequate placement appear to be unnecessary.

12. The TEE is more sensitive than the precordial Doppler to VAE and offers the advantage of also identifying rightto - left shunting of air. However , its safety during prolonged use (especially with pronounced neck flexion) is not well established. Expired nitrogen analysis is theoretically attractive.

13. However , the expired nitrogen concentrations involved in anything less than catastrophic VAE are very small and push the available instrumentation to the limits of its sensitivity. Figure presents the physiologic and monitor response to an air embolic event .

14. MONITER SENSITIVITY (VOLUME OF AIR DETECTABLE BY DEVICE) End tidal carbon dioxide level ( 0.5ml/kg) End tidal nitrogen level (0.5ml/kg) Precordial Doppler (0.05ml/kg) Transcranial Doppler (0.05ml/kg) Precordial stethoscope (1.5ml/kg) Transoesophageal Echocardiography (0.02ml/kg) Oesophageal stethoscope (1.7ml/kg) Pulmonary Artery Catheter (0.25ml/kg) Table representing the sensitivities of different investigation modalities.

15. Paradoxical Air Embolism the possibility of the passage of air across the interatrial septum via a patent foramen ovale (PFO ) or Thebesian viens in the heart which is known to be present in approximately 25% of adults, is a concern. The risk is major cerebral and coronary morbidity . However, the precise definition of the morbidity that can actually be attributed to PAE is not clear. Although the minimal pressure required to open a probe patent foramen ovale is not known with certainty , the necessary gradient may be as much as 5 mm Hg.

16. Several clinical investigations have examined factors that influence the right atrial pressure (RAP) to left atrial pressure (LAP) gradient. The use of PEEP increases the incidence of a positive RAP to pulmonary wedge pressure gradient and generous fluid administration (e.g., 2800 mL/patient versus 1220 mL/control patient reduces it.

17. The use of positive end-expiratory pressure (PEEP ), which was once advocated as a means of preventing air entrainment, was abandoned. Subsequently, the practice of more generous fluid administration for patients undergoing posterior fossa procedures evolved. However , even when mean LAP exceeds mean RAP, PAE can still occur because transient reversal of the interatrial pressure gradient can occur during each cardiac cycle.

18. Some centers have advocated performing bubble studies preoperatively with either precordial ECG or transcranial Doppler ( TCD) or prepositioning using TEE to identify patients with a PFO with a view to using alternatives to the sitting position in this subpopulation.

19. Some centers thereafter advocate the use TEE to identify paradoxical embolization intraoperatively . However, none of these practices has become a community-wide standard of care. Furthermore , because the morbid events attributable to PAE have been relatively infrequent, surgeons who are convinced that the sitting position is optimal for a given procedure are loath to be dissuaded from using it on the basis of what may seem like the very minor possibility of an injury to the patient occurring by this mechanism.

20. CLINICAL MANAGEMENT Supportive treatment forms the mainstay of clinical management for venous and arterial air emboli diagnosed in the perioperative context. Management can be further subdivided into three elements that are invariably dealt with simultaneously: • Immediate resuscitation • Prevention of further air entrainment • Efforts to remove or halt the progress of the air already entrained.

21. Immediate resuscitation is best achieved by adopting an airway, breathing and circulation approach. In an anaesthetised patient, the airway should be secured with endotracheal intubation if this has not already been done. It is important to ensure that the inspired fraction of oxygen is increased to 1.0 and adequate ventilation is maintained. This can be confirmed by arterial blood gas analysis. Nitrous oxide diffuses into air bubbles trapped in the vascular tree and, accordingly, N2O should be eliminated after a clinical VAE event to avoid aggravating the cardiovascular impact.

22. Profound cardiovascular collapse and cardiac arrest can fast ensue following large venous or arterial air embolism. Circulatory support should be commenced rapidly to increase venous pressure . These include administering fluids via large bore intravenous cannulae as well as vasopressor or inotropic support as required. If cardiac arrest is imminent or has occurred, the initial rhythm may be pulseless electrical activity or asystole , in which case advanced life support protocol for non- shockable rhythms should be followed accordingly.

23. Where paradoxical or arterial emboli are suspected, signs of cardiac ischaemia should be sought and a 12 lead ECG should be examined post-operatively . Attention should be paid to preventing further air entrainment by lowering the operative site to below the level of the heart and by stopping any process through which air could be entrained (e.g. reaming of bones during an orthopaedic surgery ).

24. Further air entrainment can also be minimised by directly compressing major blood vessels temporarily, the application of bone wax, flooding the operative sites with irrigation fluid and applying damp swabs over the suspected areas. Any gas pressurised system (e.g. pneumoperitoneum ) should be decompressed. Nitrous oxide should be discontinued as it can expand any gas filled intravascular space.

25. Attempts can be made to aspirate air through an in situ central venous catheter or an air aspiration catheter (16G multiorifice catheter that can be inserted centrally or peripherally if adequate in length). It is preferable to use a multi-orifice tipped catheter to optimise chances of aspirating the air. With a multi-orifice catheter, the tip should be sited approximately 2 cm distal from the junction of the superior vena cava and right atrium.

26. If a single lumen catheter is used, it should be positioned at 3 cm proximal to the superior vena cava-atrial junction. Radiological or intravenous ECG guidance has been recommended but are not always practical or available . To aspirate an air embolism most effectively, the trendelenburg and left lateral decubitus position are advocated because any entrained air within the heart should then theoretically float towards the right atrium and away from the coronary ostia , potentially be at a position allowing easier aspiration via a central line.

27. In practice, it is not straightforward to perform such rapid aspiration unless an aspiration catheter or central venous line is already in situ. The logistics of repositioning the patient may also be difficult

28. Treatment of Venous air embolism Immidiate resuscitative measures should be initiated following the principles of ABC. The airway should be secured, 100% oxygen saturation should be maintained, cardioplumonary resuscitation should be commenced if required. The surgeon should flood the operative site with saline to compress the wound edges.

29. Venous pressure at the operative site should be elevated by - Positioning it below the level of right atrium(if possible). Intravenous volume loading. Increasing the intrathorasic pressure with Valsulva manoeuvre , thus reducing the venous return. Jugular venous compression will reduce venous return from head and elevate cerebral venous pressure.

30. Elevating the veneous pressure helps the surgeon to identify the site of air entry. Nitrous oxide is 34 time more soluble than nitrogen and thus will diffuse in air bubble very rapidly increasing the size. Therefore the nitrous oxide should be discontinued immidiately and 100 percent oxygen is administered. 100 percent oxygen promotes the nitrogen wash out and thus reducing the size of air bubbles. Following the air embolism, air can be aspirated using central venous catheter. Even in high risk cases, central venous catheter can be inserted prior to surgery.

31. The optimum site for the tip of catheter is within the right atrium 2cm below the junction of superior vena cava. The proper placement of centra venous catheter can be confirmed radiologically or by ECG changes. The left lateral decubitus postion is helpful in massive air embolism. Inotrops can be useful in increasing the cardiac output and systemic blood pressure.

32. Which Patients Should Have a Right Heart Catheter? Essentially , all patients who undergo sitting posterior fossa procedures should have a right heart catheter placed. Although life-threatening, VAE is relatively uncommon, a catheter that permits immediate evacuation of an air-filled heart is occasionally the sine qua non for resuscitation .

33. The latitudes are much wider with the nonsitting positions, and it is frequently appropriate, after a documented discussion with the surgeon, to omit the right heart catheter. The perceived risks of VAE associated with the intended procedure, and the patient’s physiologic reserve are the variables that contribute to the decision. Microvascular decompression of the fifth cranial nerve for tic doloureux or the seventh cranial nerve for hemifacial spasm are examples of procedures for which the right heart catheter is usually omitted.

34. The essentially horizontal semilateral position and the very limited retromastoid craniectomy that is required have resulted (at our institution) in a very low incidence of Doppler-detectable VAE. One should know the local surgical practices, particularly with respect to the degree of head-up posture, before becoming casual about omitting the right atrial catheter .

35. With regard to the Jannetta procedure, the necessary retromastoid craniectomy is performed in the angle between the transverse and sigmoid sinuses, and venous sinusoids and emissary veins in the suboccipital bone are common. If this procedure is performed with any degree of head-up posturing, the risk of VAE may still be substantial.

36. Which Vein Should Be Used for Right Heart Access ? Although some surgeons may ask that neck veins not be used , a skillfully placed jugular catheter is usually acceptable . In a very limited number of patients, high ICP may make the head-down posture undesirable . In others, unfavorable anatomy with an increased likelihood of a difficult cannulation and hematoma formation may also encourage the use of alternate access sites.

37. Positioning the Right Heart Catheter The investigation of Bunegin and colleagues suggested that a multi- orificed catheter should be located with the tip 2 cm below the superior vena caval –atrial junction and a single orificed catheter with the tip 3 cm above the superior vena caval –atrial junction. Confirmation of right heart placement can be accomplished by (1) radiography or ( 2) intravascular electrocardiography(ECG).

38. Although there is no literature to support the practice, with catheter access via the right internal jugular vein , a measured placement to the level of the second or third right intercostal space should suffice when the catheter passes readily. The intravascular electrocardiography technique makes use of the fact that an ECG “electrode ” placed in the middle of the right atrium will initially “see” an increasing positivity as the developing P-wave vector approaches it, and then an increasing negativity as the wave of atrial depolarization passes and moves away from it. The resultant biphasic P wave is characteristic of an intraatrial electrode position .

39. The technique requires that the CVP catheter become an exploring ECG electrode. This is accomplished by filling the catheter with an electrolyte solution (bicarbonate is best) and attaching an ECG lead (the leg lead if lead II is selected) to the hub of the CVP catheter . Commercial CVP kits with an ECG adapter are available. The ECG configurations that will be observed at various intravascular locations. To minimize the microshock hazard, a battery-operated ECG unit is preferable, and any unnecessary electrical apparatus should be detached from the patient during catheter placement.

40. RISK FACTORS FOR ARTERIAL AIR EMBOLISM Risk factors for thromboembolism, the major cause of arterial embolism, include disturbed blood flow (such as in atrial fibrillation and mitral stenosis), injury or damage to an artery wall, and  hypercoagulability  (such as increased platelet count ).  Mitral stenosis poses a high risk of forming emboli which may travel to the brain and cause stroke .   Endocarditis increases the risk for thromboembolism ,  by a mixture of the factors above .

41. Atherosclerosis in the aorta and other large blood vessels is a common risk factor ,  both for thromboembolism and cholesterol embolism. The legs and feet are major impact sites for these types .  Thus, risk factors for atherosclerosis are risk factors for arterial embolisation as well which are as follows: advanced age . cigarette smoking hypertension (high blood pressure) obesity Hyperlipidemia, e.g. hypercholesterolemia, hypertriglyceridemia, elevated lipoprotein (a) or  apolipoprotein B, or decreased levels of HDL cholesterol )

42. diabetes mellitus Sedentary lifestyle stress Other important risk factors for arterial embolism include: recent surgery  (both for thromboembolism and air embolism) previous stroke or cardiovascular disease a history of long-term intravenous therapy  (for air embolism) Bone fracture (for fat embolism) A  septal defect of the heart makes it possible for  paradoxical embolization, which happens when a clot in a vein enters the right side of the heart and passes through a hole into the left side. The clot can then move to an artery and cause arterial embolisation

43. Prevention of Air Embolism Avoid sitting position unless essential. Elevate the head only as much as necessary. Ensure the adequete blood volume to maintain a positive Central venous pressure. Small amount of PEEP(5 – 10 cmH20) may reduce the risk of air entrainment. Stop N2O if in use and increase the FiO2 to 1.0

44. Treatment of Arterial Air Embolism As in the venous air embolism, maintaining the (1)Airway(2)Breathing(3)Circulation will be the first line management for arterial air embolism. The treatment of choice for arterial air embolism is hyperbaric oxygen supplimentation . The administration of hyperbaric 100% oxygen provides hyperoxia and large pressure gradients for oxygen to diffuse into and nitrogen diffuse out of the emboli.

45. Discussion Air embolism can present as both brady - or tachyarrhythmias . Trans- oesophageal echocardiography has the highest sensitivity for detecting air embolism . Mill-wheel murmur is often only present in cases with large air embolism. It is also a late sign with low sensitivity and specificity.

46. REFERENCES : Miller Morgan British Journal Of Anaesthesia Oxford Handbook of Anaesthesia