The sitting position; monitoring, diagnosis and treatment of air embolism

10

The sitting position; monitoring, diagnosis and treatment of air embolism P. M. B R O D R I C K

The anaesthetist faces major problems when planning to anaesthetize a patient undergoing a neurosurgical procedure in the sitting position, particularly postural hypotension and air embolism. These problems are well recognized and documented, but despite this, the sitting position still maintains a level of popularity amongst surgeons, which requires the anaesthetist to be prepared for any of these hazards (Matjasko et al, 1985; Frost, 1984; Young et al, 1986). Recent work has suggested that the sitting position is safer than has previously been reported (Cucchiara, 1984a), and that the outcome of surgery is not affected by the patient's position (Oliver and Cucchiara, 1986). Overall, the sitting position, when compared to alternative positions, favours better physical access to the operative site, directly behind the wound rather than to one side, and improved gravitational drainage of blood and debris leaving a clearer surgical field. Because the intrathoracic pressure during ventilation tends to be lower in the sitting position than when the patient is prone, the venous distension and spinal cord pulsation tend to be less. With the head supported by a head ring or pin type head holder, more flexion of the head is possible than in the prone position. From the anaesthetist's point of view, the sitting position enables him or her to view the face with relative ease, because monitoring evoked twitch responses from stimulated cranial nerves and access to the chest wall for monitoring purposes is relatively unobstructed (Martin, 1978; Freuchen, 1959). The disadvantages of the sitting position include postural hypotension and air embolism in particular, but also cardiac arhythmias from brain stem stimulation, pneumocephalus and swelling of the face and tongue. CARDIOVASCULAR EFFECTS OF THE SITTING POSITION The normal cardiovascular system responses due to the change from the supine to the sitting position were described by Ward (1966) who subjected healthy, fully conscious volunteers to changes in posture whilst measuring some cardiovascular parameters. The stroke volume decreased by 20% and the heart rate increased by 18%. The resultant change in the cardiac output Bailli~re's ClinicalAnaesthesiology--Vol. 1, No. 2, June 1987

419

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was a 10% fall, but left the mean arterial pressure unchanged. Marshall et al (1983) compared the cardiovascular effects of four different anaesthetic techniques and observed the response of moving from the supine to the seated position. In awake patients (supine to upright) they found increases in heart rate, mean arterial pressure, systemic vascular resistance and arterial PO2 and a decrease in stroke volume indices and pulmonary wedge pressure, leaving the right atrial pressure, pulmonary artery pressure and cardiac index unchanged. Further changes from control values occurred following anaesthesia and on the change in posture, depending on the anaesthetic technique used. These alterations returned towards control values following the commencement of surgery. Albin et al (1974) and Dalrymple et al (1979) noted decreases in the cardiac index and arterial oxygen transport and an increase in the systemic vascular resistance and the mean arterial pressure. These are compensatory mechanisms resulting from the change in posture during anaesthesia (Martin, 1978). The change in arterial oxygenation was probably due to the decreased cardiac output. Tindall et al (1967) found a significant decrease in the cardiac output and a 14% fall in carotid artery flow when anaesthetized subjects (PaCO2 of 40 mmHg) were placed in the sitting position. These changes were accentuated by hyperventilation (PaCO2 of 21mmHg) decreasing carotid artery flow by 48% (from control) in the sitting position, resulting from an increase in cerebrovascular resistance from the lowered carbon dioxide level. In clinical practice, these changes in cardiovascular status are not always readily apparent (Tausk and Miller, 1983). Albin et al (1976) found that 32% of their patients experienced a 10-20 mmHg drop in blood pressure when moved into the sitting position, which correlated to ASA status, whereas 10% actually became hypertensive during the same manoeuvre. Both Millar (1972) and Young et al (1986) recorded an incidence of hypotension of between 5 and 10%.

Prevention of postural hypotension A suitable anaesthetic technique, e.g. a morphine/nitrous oxide maintenance technique following a thiopentone induction, suxamethonium for intubation and pancuronium for muscular relaxation has been shown to produce the least change in cardiovascular parameters (Marshall et al, 1983) when compared with a nitrous oxide/enflurane or halothane combination. Anaesthetic agents that are potent vasodilators and cardiac depressants add to the problems of maintaining a reasonable cerebral perfusion, by increasing venous pooling and decreasing cardiac output. Preloading with intravenous fluids just prior to moving the patient from the supine to the sitting position has been recommended (Shapiro and Aidinis, 1975). In their study, Matjasko et al (1985) used between 7-14 ml/kg of balanced salt solutionprior to the change in posture. Vasopressors, by increasing peripheral sympathetic tone, heart rate and cardiac contractility have been suggested to prevent postural hypotension (Shapiro and Aidinis, 1975). Millar (1972) used an infusion of phenylephrine in 42% of the cases paralysed with tubocurarine, usually after

MONITORING, DIAGNOSIS AND TREATMENT OF AIR EMBOLISM

421

intermittent positive pressure ventilation (IPPV) was first instituted. Tinker and Vandam (1972) recommended a combination of leg bandaging, intravenous fluids and vasopressors as the most suitable technique. The use of vasopressors may cause unwanted bleeding in the operation site and poor peripheral blood flow (Martin, 1970b). Compression, by leg bandages or antigravity suit. Several authors have suggested the use of bandages on the legs to promote venous return, to help prevent postural hypotension (Albin et al, 1974; Tinker and Vandam, 1972). Dalrymple et al (1979) and Geevarghese (1977) have stated that leg bandages do not prevent the circulatory changes that result from a patient's postural change and have suggested that an antigravity suit might be more effective than vasopressors and leg bandages. The bandages do not take advantage of the large abdominal reservoir of blood that is compressed by the antigravity suit. In aviation medicine, the importance of abdominal compression has been shown to obtain maximum protection against gravitational acceleration (Wood and Lambert, 1952; Burton and Krutz, 1975). The combination of leg and abdominal compartment inflation has more than double the protective value of leg compression alone. Application of an antigravity suit to prevent hypotension has been suggested by several workers (Auer, 1976; Crile, 1909; Gardner and Dohn, 1956). Using a suit inflation pressure of 25 mmHg, Freuchen (1959) showed that the volume of intravenous fluids and blood infused and use of vasopressors were less in those sitting patients with the antigravity suit fitted, when compared to those with elastic leg bandages. Tinker and Vandam (1972) stated that there was no advantage in using an antigravity suit (the plastic wrap around Gardner model, 1956); indeed, it may cause peripheral nerve injuries, particularly to those nerves crossing the iliac crests and the neck of the fibula. Application of the suit may possibly apply uneven pressure, causing cutaneous ischaemia (Tinker and Vandam, 1972b). However, these problems have not been reported with the aviation type of suit as used by other workers (Hewer and Logue, 1962; Freuchen, 1959). The combination of a cardiovascularly stable anaesthetic technique, combined with lower body compression, enables smaller volumes of intravenous fluids to be given and optimizes control of hypotension.

Complications of the sitting position Pressure on the face and eyes may arise from the horseshoe ring used to support the head during the operation (Tausk and Miller, 1983). However, this may be overcome by careful fixation of the head prior to the commencement of surgery. Another solution is to use the skull-pin type of head fixation (Martin, 1970a). Several authors (Ellis et al, 1975; Tattersall, 1984) have reported cases of facial swelling resulting from prolonged operation time and diminished blood flow to the head during surgery due to deliberate hypotension. One patient had swelling of the tongue, lips and face postoperatively and developed a progressively worsening respiratory distress and stridor requiring reintubation and ventilation. The cause of the swelling was probably

422

P.M. BRODRICK

kinking of the internal jugular vein when the neck was maximally flexed, causing thrombosis and partial or complete obstruction of the vessel. Tension pneumocephalus has been described following posterior fossa surgery in the sitting position presenting postoperatively as a deterioration in the neurological status (Kitahata and Katz, 1976). Standefer et al (1984) had eight patients develop symptoms attributable to pneumocephalus. Most were confirmed on a postoperative skull x-ray or CT scan and resolved in a few days. The incidence of other complications as reported by Standefer et al (1984) was very low, but included bilateral subdural formation (1.3%) and peripheral nerve injury (0.82%). The latter may have been caused by reduced muscle tone, allowing stretching or compression of the nerve resulting in ischaemia of the vas nervorum, possibly arising from bandages on the legs. Two patients in the same series suffered a traumatic haemarthrosis and dislocation of the elbow and five patients developed significant cutaneous lesions due to the prolonged length of the procedure. The majority of these problems can be overcome by scrupulous attention to padding vulnerable areas by the anaesthetist during positioning. AIR EMBOLISM

When the patient is in the sitting position or in a position with the head tilted up, a 5 cm gradient of pressure between the upper pole of the wound and the right atrium is all that is required to allow the passage of air into the venous circulation (Albin et al, 1983). There are several factors which contribute to the effect of any air embolism.

Volume of air entrained. A large volume within the pulmonary circulation may exceed the lung's capacity to dissipate the air (Butler and Hills, 1979). Speed of entry. Wolffe and Robertson (1935), and Richardson et al (1937) showed experimentally that the morbidity was related to the rate of entry of air rather than the total volume. Addornato et al (1978) showed in dogs that slow infusions (0.4-0.6 ml/kg/min) caused the air to be spread throughout the cardiopulmonary circulation and caused the pulmonary artery pressure to rise, with a fall in the peripheral resistance and cardiac output. During bolus infusions of air, a large rise in the central venous pressure with a fall in pulmonary artery pressure occurred and this was possibly due to a build up of air solely in the right side of the heart.

Position of the body. Elevation of the head exacerbates the problem (Senn, 1885).

Efficacy of the respiratory mechanism. Prevention of deep inspiration during spontaneous ventilation at the time of the embolism is important (Durant et al, 1947; Senn, 1885).

423

MONITORING, DIAGNOSIS AND TREATMENT OF AIR EMBOLISM

The incidence of reported air embolism depends on the monitoring methods used to detect the embolus, and the type of procedure being undertaken, suboccipital craniectomy being particularly susceptible (Matjasko et al, 1985; Standefer et al, 1984). Table 1 shows the variable incidence in several large studies. Table 1. Incidence of venous air embolism. Study

Year

Numbers

(%)

Albin et al Bedford et a! Matjasko et al Michenfelder et al Millar Standefer et al Voorhies et al Y o u n g et al

1976 1981 1985 1969 1972 1984 1983 1986

400 100 554 418 110 332 81 255

25 35 23 6 2 7 50 30

Most episodes occur early on during the procedure (73-76%) (Albin et al, 1976; Standefer et al, 1984), and only 18-25% of the episodes occur late or during closure (Albin et al, 1976; Standefer et al, 1984). Patients are most at risk from an air embolism during the stripping of muscles and fascia (Leivers et al, 1971), drilling of the skull (Ericsson, 1964), or during fascial layer closure (O'Higgins, 1970). The air appears to enter via the diploic veins, suboccipital venous plexus, occipital emissary veins, dural sinuses and veins in a tumour itself. Other sources of air embolism have been reported and include air entry from the wounds of a pin-type skull fixation device (Cabezudo et al, 1981) and from burr holes (Edelman and Wingard, 1980), but many episodes occur without positive identification (Merrill et al, 1982) of the source, as much as 63% in one study (Matjasko et al, 1985). The air enters the circulation and travels down the superior vena cava into the right atrium and ventricle. The change in the flow and increased turbulence caused by the presence of the air around the pulmonary valve is thought to cause the characteristic'mill wheel murmur' (Ericsson et al, 1964). There it tends to mix with the blood present and forms a foam which if significant enough may cause an outlet obstruction of the pulmonary artery. However, this is not usually the case, as much of the air/blood mixture is expelled into the pulmonary arterial tree. The rise in pulmonary artery pressure associated with the movement of the air/blood mixture is greater than can be accounted for by obstruction alone (Addornato et al, 1978), but whether the mechanism is humoral or neural in origin is unknown. Once in the pulmonary vessels, the air can cause refex bronchoconstriction, pulmonary oedema and may, if the quantities are large enough, cross into the systemic circulation (Butler and Hills, 1979). Thus threshold for the tung to filter air is 0.30 ml/kg/min (Butler and Hills, 1985), and is affected by the presence of anaesthetic agents (halothane and isoflurane) (Katz et al, 1986), and bronchodilators which generally lower the threshold, whereas nitrous oxide (Butler et al, 1985b) and PEEP tend to raise it (Butler et al, !986c). The

424

P.M. BRODRICK

physical blockage of pulmonary vessels by air may cause an increased V/Q mismatch (Shapiro and Aidinis, 1975), and a decrease in the removal of carbon dioxide will decrease the end tidal carbon dioxide concentration (Pearl and Lawson, 1986). Venous air embolism has occurred in other positions during neurosurgery. Shenkin and Goldfedder (1969) reported a case occurring in the prone position with the head 10cm above the heart and in the presence of a negative phase in the ventilatory cycle. Albin et al (1979) noted that 36% of the episodes of air embolism occurred in other positions and Harris et al (1985) demonstrated air embolism in supine infants tilted 5~ head up. Other situations where air embolism has been reported include ear, nose and throat surgery involving the veins in the head and neck (Senn, 1885), total hip replacement (Anderson, 1983), liver and vena cava lacerations, placenta praevia, pneumothorax, otoscopic air insufflation, pneumorbitography (Newfield, 1980), central venous catheter insertion/disconnection (Ordway, 1974) and during cardiopulmonary bypass surgery (Mills and Ochsner, 1980). Prevention of air embolism is best achieved by prophylactic measures involving raising the venous pressure. The antigravity suit (G-suit) has been suggested as a potential method of increasing the central venous pressure to prevent an air embolism by several authors (Freuchen, 1959; Geevarghese, 1977). Contrasting evidence exists for the ability of an antigravity suit to maintain a consistent effect on the right atrial pressure. One study (Ingram and Brodrick, 1986) has shown that by inflating the suit to 60mmHg, the right atrial pressure was raised by 7.0 mmHg and maintained to 78% of this increase although inflated for a mean time of 115 minutes. Figure 1 demonstrates the result of inflating an antigravity suit. Further work with the medical antishock trouser (MAST) has shown that when inflated to 50 cm water pressure, the rise in right atrial pressure was maintained whilst the suit was still inflated (Toung, 1985). A different study found a reduced incidence of venous air embolism in the presence of an inflated MAST whilst using an augmented intravenous fluid regimen (Beloucif et al, 1986). Martin (1970b) using a different type of suit (a wrap around plastic model) inflated to 30 mmHg was unable to sustain the rise in right atrial pressure. Positive end expiratory pressure (PEEP) has been suggested as a prophylactic method.of raising the venous pressure. Hewer and Logue (1962) used a loaded spirometer in the anaesthetic circuit on spontaneously breathing patients and adjusted the weight to provide the optimum conditions for surgery. An antigravity suit was used to counteract the cardiovascular changes caused by the PEEP. The combination of PEEP and abdominal compression has raised dural venous sinus pressure more effectively than single application of either (Hibino and Matsuura, 1985). Lee et al (1981) used 10 cm water of PEEP throughoUt surgery and the incidence of venous air embolism was reduced when compared to a control group. Other authors have had similar experiences (Gilsanz and Avello, 1982; Toung et al, 1984) using a variety of positive pressures, but venous air embolisms have still been detected in the presence of PEEP (Voorhies et al, 1983).

425

MONITORING~ DIAGNOSIS AND TREATMENT OF AIR EMBOLISM B

!

f

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100

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Bimanual compression of the neck has been recommended (Tausk and Miller, 1983), but it is awkward to reach under the surgical towels to squeeze the neck in a relatively uncontrolled manner. A device has been developed that may make this easier, consisting of an inflatable tourniquet placed around the neck of the patient prior to the commencement of surgery. The

426

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tourniquet is inflated at those times when an air embolism is most likely to occur, or after an air embolism has been diagnosed, to prevent further entrainment. However, the tourniquet may produce considerable congestion in the operating field causing a rise of intracranial tension (Pfitzner and McLean, 1985; Sale, 1984). Leg bandaging has been suggested by some authors (Albin et al, 1974; Matjasko et al, 1985) as a method of improving venous return and reducing venous pooling. However, the Same limitations arise as were discussed in the section on hypotension. The use of intravenous fluids may help to raise the right and left atrial pressures (Colohan et al, 1985) but on their own are unlikely to be sufficient to prevent an air embolism. However, their use in conjunction with a M A S T suit does seem to be effective (Beloucif et al, 1986).

427

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Figure 2. Two examples of brain stem manipulation, causing marked bradycardia, but without a sustained drop in the PE'CO2.

Differential diagnosis of air embolism Brain stem retraction or compression is the other likely cause of arrhythmias or a sudden drop in heart rate and blood pressure during this type of surgery. The most significant difference between the two diagnoses is the absence of a sustained drop in the end tidal carbon dioxide. Figure 2 shows two examples of the typical response in arterial and venous pressures and end tidal carbon dioxide to brain stem manipulation.

428

P.M. BRODRICK

MONITORING T h e ideal characteristics of a device to detect intravascular air should be the following: a) sensitive e n o u g h to enable an early diagnosis to be m a d e but not so sensitive as to cause unnecessary alerts, b) able to indicate the quantity of air entrained so as to distinguish b e t w e e n a small but c o n t i n u o u s e n t r a i n m e n t of air as o p p o s e d to a s u d d e n bolus, c) able to detect w h e n an e m b o l i s m has finished. N o o n e device satisfies these criteria completely, but it is possible by combining m o r e t h a n o n e device to achieve a satisfactory balance. Table 2 indicates s o m e of the available devices and their relative sensitivities.

Precordial Doppler This is a sensitive device (Michenfelder et al, 1972; G i l d e n b e r g et al, 1981), as used in m a n y large studies (Matjasko et al, 1985; Standefer et al, 1984). T h e s o u n d m a d e by the device during an air e m b o l i s m has b e e n described as 'chirping' or muffling the n o r m a l heart sounds. It c a n n o t d e t e r m i n e the quantity of air e n t r a i n e d and is p r o n e to give false positives, but will give an indication w h e n an e m b o l i s m has finished. T h e r e can be difficulty in positioning the d e t e c t o r (Michenfelder et al, 1972b), but a test dose of c a r b o n dioxide injected t h r o u g h a right atrial catheter m a y be helpful

Table 2. Relative sensitivities of the available monitoring devices. Device Transoesophageal echocardiography Transoesophageal Doppler Precordial Doppler PE'T carbon dioxide Airway pressure Pulmonary artery pressure Central venous pressure ECG Arterial oxygen Transcutaneous oxygen Respiration Arterial carbon dioxide Mean arterial pressure Transcutaneous carbon dioxide Oesophageal stethoscope

Quantity of air (ml/kg)

Reference

0.05--43.19 Glenski et al (1986) 0.05-0.2 Martin and Colley (1983) 0.12-0.24 English et al (1978) Glenski et al (1986) 0.18-0.63 Edmonds-Seal et al (1971) Glenski et al (1986) 0.2 Sloan and Kimovec (1986) 0.25-0.61 English et al (1978) Glenski et al (1986) 0.4-2.0 English et al (1978) 0.6-2.0 Edmonds-Seal et al (1971) English et al (1978) 0.71-0.75 English et al (1978) Glenski et al (1986) 0.76 Glenski et al (1986) 0.8 Edmonds-Seal et al (1971) 1.15 Glenski et al (1986) 1.16-2.0 English et al (1978) Glenski et al (1986) 1.54 Glenski et al (1986) 2.0 English et al (1978)

MONITORING~ DIAGNOSIS AND TREATMENT OF AIR EMBOLISM

429

(Tinker et al, 1975). It is highly susceptible to diathermy interference and has an inbuilt suppression circuit which cuts out the Doppler signal during diathermy use. This leads to a loss of its early warning capability during diathermy of a vessel entraining air. It is also susceptible to the electrical interference from fluorescent tubes in x-ray viewing boxes. Transoesophageal Doppler

This has been used experimentally in dogs (Martin and Colley, 1983) and is suggested as an alternative to the precordial Doppler. It is not affected by chest shape or size to the same extent as a precordial detector. Because of its wide arc of view it should be easier to position and it is less likely to suffer attenuation because of its proximity to the heart. Its optimum position to detect venous air emboli was found to be at the level of the superior vena cava above its junction with the right atrium. Contrast echocardiography

Transoesophageal echocardiography, either M-mode or the two-dimensional (2D) technique, has been used to detect air embolism in all the chambers of the heart and for the preoperative and intraoperative diagnosis of a patent foramen ovale (Cucchiara et al, 1984; Furuya et al, 1983; Sato et al, 1986), which is an advantage over the Doppler. The 2D echo allows a larger tomographic field to be visualized, permitting better appreciation of the anatomy. The sensitivity of this device is slightly more than the Doppler (Glenski et al, 1986), and it may be possible to quantify the embolism by contrast intensity and duration (Roewer et al, 1985), though this has been disputed (Glenski et al, 1986). The Doppler and 2D echo may interfere with each other when used together (Cucchiara et al, 1984). Routine use of these devices will require considerable time in gaining expertise and will cost large sums of money. End tidal carbon dioxide

The infrared analyser is capable of giving a quantitative estimate of the size of the embolus (English et al, 1978; Glenski et al, 1986), falling as a result of decreased carbon dioxide excretion. The response may be sustained (Brechner and Bethune, 197t). It does not suffer from diathermy or electrical interference and its use has been recommended by Symons and Leaver (1985). Central venous pressure

This tends to rise slowly following the embolism from blockage of the pulmonary outflow tract. Measurement of the venous pressure is probably not as useful as the presence of the catheter itself. The role of the right atrial catheter continues to be debated (Frost, 1984), despite its ability to be life saving during a large bolus of air (Michenfelder, 1981). Accurate positioning

430

~'. M. BRODRICK

of the catheter tip is the main problem and several methods have been described to position the catheter at the junction of the lower part of the superior vena cava and the apex of the right atrium (Bunegin et al, 1981), the best position for aspiration. Martin (1970c) described a technique for the accurate placement of a saline-filled right atrial catheter by using it as an exploring electrode. Using an antecubital fossa vein the characteristic inverted 'P' wave changes to a more 'W' like appearance when the catheter reaches the junction of the superior vena cava and the right atrium. A final check with the ECG should always be made with the patient in the final position. A success rate of 76% in a relative short space of time appears possible (Colley and Atru, 1984). Multi-orificed catheters are not as easy to position in this manner, as the ECG tracing is not of the same quality (Michenfelder, 1981). When the patient is moved from the supine to the sitting position the catheter will tend to shift its position, moving further into the right side of the heart (Lee et at, 1984). Other positional techniques include chest x-ray with and without contrast. The success rate of aspirating these catheters is variable and this may arise from the positioning difficulties. The volumes of air aspirated from right atrial catheters has varied from 2-1200 ml (Michenfelder et al, 1969), 65% of those aspirated were less than 50 ml. The removal of air will reduce the quantity available for transpulmonary passage (Michenfelder, 1981).

Pulmonary artery pressure This tends to show an early rise, caused by small volumes of air initiating a marked increase in pulmonary vascular resistance (English et al, 1978) and may rise as high as 11 mmHg (Bedford, 1981). The size of the increase may give an indication of the quantity of air entrained (English et al, 1978). The catheter may also be used to detect brain stem related changes in haemodynamic variables and to identify those patients who might be at risk from paradoxical air embolism through a probe patent foramen ovale, in whom the right atrial pressure may become higher than the pulmonary capillary wedge pressure. Air may be aspirated from the distal opening of the catheter from further inside the pulmonary arterial outflow tract and from the right atrium by the proximal opening. Attempts to aspirate these catheters may be disappointing (Bedford et al, 1981), partly from being unable to obtain the best position (Sink et al, 1976).

Intra-arterial pressure An early fall in blood pressure soon after an air embolism has occurred is quite common (Marshall, 1965). Hypotension was marked (falling by more than 25% of previous value) in 17 out of 40 episodes in one series (Michenfelder et al, 1969), but this response can be variable and not sufficiently sensitive enough for early diagnosis.

M O N I T O R I N G , D I A G N O S I S A N D T R E A T M E N T OF AIR EMBOLISM

431

Electrocardiography Lead I is an appropriate lead to display for routine monitoring (Lewis and Rees, 1964), but changes in the tracing are unreliable. Buckland and Manners (1976) found ECG changes in 40% of those cases who had air embolism confirmed by the Doppler. The most common changes seen are in the P and T waves, R bundle branch block, ventricular abnormalities and ST depression (Tateishi, 1972; Millar, 1972).

Oesophageal stethoscope This has been the traditional monitoring method, being cheap and easy to position, but it tends to occupy one person completely. Its continuous use has been strongly recommended (Marshall, 1965). The description of the sound heard during an air embolism is like 'a mill wheel' (Durant et al, 1947) or 'drum like', but it tends to be rather insensitive (Buckland and Manners, 1976) when compared to other methods. Other monitoring aids recently investigated include airway pressure (Sloan and Kimovec, 1986) and transcutaneous oxygen and carbon dioxide monitors (Glenski et al, 1986). Further evaluation is required to determine their individual usefulness. Figure 3 shows two examples of venous air embolism, showing the effect on arterial and venous pressures and end tidal carbon dioxide.

TREATMENT OF AIR EMBOLISM When an air embolism has been suspected or detected by the monitoring apparatus, action should be taken immediately. One of the factors in the successful resuscitation of patients was the speed of diagnosis and treatment (Ericsson et al, 1964). Inform the surgeon so that a check of the operation site can be made, to ascertain the point of entry of the air (Michenfelder et al, 1969). The whole wound should be flooded with saline or covered in a saline-soaked swab, and the edges of any exposed bone should be sealed with bone wax. Identification of the offending vessel may be improved by raising the venous pressure either locally or systemically. Controversy has arisen as to whether or not it is reasonable to raise the venous pressure (by means of antigravity suit inflation, PEEP application or neck compression) to minimize the further entry of air. A rise in the venous pressure may lead to a higher right than left atrial pressure and may increase the incidence of paradoxical air embolism (Perkins and Bedford, 1984). Bimanual neck compression by hand (Michenfelder et al, 1969; Tausk and Miller, 1983), by inflation of a previously positioned inflatable neck tourniquet (Sale, 1984) or a neck tie of Paul's tubing (Buckland and Manners, 1976) may help to identify the site of entrainment by raising the local venous pressure. Aspiration of a previously positioned right atrial catheter may allow the removal of some of the entrained air (Senn, 1885), although some air will

432

v.M. BRODRICK B

C

have already passed into the pulmonary vessels. A pulmonary artery catheter will be able to reach air that has passed further into the pulmonary outflow tract. Withdrawal of nitrous oxide (Munson, 1971; Nunn, 1959) and the administration of 100% oxygen will help minimize the expansion in size of the air bubbles within the blood. Since nitrous oxide is 30 times more soluble than nitrogen in blood, a larger volume of nitrous oxide will replace the

433

MONITORING, DIAGNOSIS AND TREATMENT OF AIR EMBOLISM A

C

1

1 1

B

P mm~

~~~~"

,,,, l ikr ' CVP

30

f

mmHg '

'

1 minute

ETC02

Figure 3. Two examples of air embolism. A t A: a change in the Doppler signal was noticed. A t B: an antigravity suit was inflated. A t C: Air was aspirated from a right atrial catheter.

nitrogen in the bubbles as nitrogen goes into the blood, leading to an expansion in the bubble size. Tolerance to a denitrogenated air embolism is increased when compared to air (Steffey et al, 1974). The reintroduction of nitrous oxide following an air embolism has been suggested as a test for the complete pulmonary excretion of the embolized air (Shapiro et al, 1982). If the changes indicative of an air embolism recur, then the nitrous oxide should be withdrawn once again. Butler et al (1985b) have demonstrated

434

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that nitrous oxide raises the lung's threshold for the filtration of air and thus its presence may help prevent paradoxical air embolism. It is interesting to note that Matjasko et al (1985) failed to implicate nitrous oxide in increasing the morbidity of the sitting position in their study. After the initial therapeutic manoeuvres the patient should be treated symptomatically. If hypotension occurs, then a rapid infusion of intravenous fluids, preferably colloid, should be given. Particular attention should be paid to children as hypotension occurs more frequently than in adults (Matjasko et al, 1985). The judicious use of a vasopressor such as ephedrine 15 mg intravenously and 15 mg intramuscularly can be used, especially if hypotension persists. If the patient fails to respond to this therapy, then repositioning the patient, preferably in the left lateral position (Hamby and Terry, 1952), should be the next course of action (Marshall, 1965). The air within the heart will then tend to gravitate upwards, towards the right atrium where it can be aspirated via a right atrial catheter. It is also extremely difficult to perform adequate external cardiac massage with the patient still seated, so if the patient has no or low cardiac output, repositioning is mandatory. COMPLICATIONS OF AIR EMBOLISM Paradoxical air embolism

A patent foramen ovale (PFO) is present in 20-35% of the population (at post-mortem examination) (Edwards, 1968), so venous air embolism is hazardous in these patients if the right atrial pressure is higher than the left, as it may lead to systemic embolism (Albin, 1984; Fischler et al, 1984; Gronert et al, 1979). These conditions may exist if there is high venous pressure, particularly if PEEP and IPPV are used (Perkins and Bedford, 1984). The risk is increased by prolonged and repeated venous air embolism but may also occur across the pulmonary circulation without the presence of a PFO (Butler et al, 1983a; Marquez et al, 1981). The incidence has been reported in one series as 2.3% of all those patients having venous air embolism (0.5% of all patients) (Matjasko et al, 1985). Air has been reported in the cerebral and coronary arteries, presenting with ST elevation or depression, or widening of the QRS complex (Clayton et al, 1985). Air has also been found in the coronary vessels at post-mortem (Buckland and Manners, 1976). Cerebral artery air embolism can lead to perioperative epileptogenic activity on a cerebral function monitor (Clayton et al, 1985), poor recovery of neurological function as a result of ischaemia (Gronert et al, 1979), or may be seen on a postoperative CT scan (Perkins-Pearson et al, 1982). Contrasting evidence exists for likelihood of increasing a paradoxical air embolism by having a high right atrial pressure, so that if the latter exceeds the pulmonary arterial wedge pressure then the chances of a paradoxical embolism are more likely. Pearl and Lawson (1986) have shown in dogs, and Zasslow et al (1986) in humans have shown that the interatria! pressure

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gradient (between right and left atria) is unchanged in relation to either the presence of PEEP or after a venous air embolism and concluded that it was unlikely that PEEP would increase the risk of a paradoxical air embolism. Butler et al (1986c) have shown that PEEP raises the threshold of the lung for the filtration of air and is unlikely to increase the incidence of paradoxical air embolism. Perkins et al (1984a, 1980b) however, using PEEP, and Mehta and Sokoll (1981) using a model of venous air embolism, have demonstrated slightly larger rises in right than left atrial pressure with the application of PEEP, indicating that this might increase a paradoxical air embolism by increasing the interatrial pressure gradient. Prevention of paradoxical air embolism Contrast echocardiography provides a safe, non-invasive method of detecting right-to-left shunts preoperatively (Higgins et al, 1984), so that those patients who have a PFO detected are not operated on in the sitting position. The detection rate can be increased by coughing and the performance of the Valsalva manoeuvre which increases the right-to-left gradient pressure. Overall, the detection rate of PFO in one study (Guggiari et al, 1985) was less (13%) than would have been expected in post-mortem findings. Fluid loading peroperatively has been shown to increase pulmonary artery pressure sufficiently to prevent a right-to-left gradient developing across the atria (Colohan et al, 1985; Perkins-Pearson et al, 1982). Using two intravenous fluid regimens (one normal, one augmented), the authors demonstrated that patients in the augmented fluid group did not develop right atrial pressure higher than pulmonary capillary wedge pressure, compared to the normal fluid regimen patients. Thus the risk for paradoxical air embolism was greater in the normal intravenous fluid regimen group. However, the data from the earlier part of the operation, when the occurrence of air embolism tended to be more common, showed that there was no difference between the two regimens (Colohan et al, 1985). Perfluorocarbon (Tuman et al, 1986) given prophylactically has been suggested, as the solubility of gases in it are generally higher than in blood, therefore reducing the size of the embolus. The incidence of paradoxical air embolism in spite of the frequency of venous air embolism is low, even in the presence of a moderately raised right atrial pressure. This supports the practice of prophylactic measures to prevent venous air embolism from occurring. Other complications Hypoxia secondary to bronchoconstriction as the entrained air blocks pulmonary vasculature (Shapiro and Aidinis, 1975) is a potential hazard and this may lead to pulmonary oedema. Clinical reports of pulmonary oedema following air embolism have been published by Pershau et al (1976) and Ishak et al (1976) but it is not a common complication of air embolism. The mechanism triggering pulmonary oedema is as yet not fully understood.

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Hypotension quite commonly occurs following air embolism and may be accompanied by ventricular ectopic beats and tachycardia (Newfield, 1980). If air reaches the coronary circulation it may precipitate ventricular fibrillation and cardiac arrest. Death as a direct result of air embolism is fortunately uncommon; none of the deaths in the Young et al (1986) or the Standefer et al (1984) series were attributable to venous air embolism. Operative mortality was correlated to preoperative ASA status. In an earlier study by Ericsson et al (1964), a significant proportion (28%) of all the patients that were treated for venous air embolism died. The overall morbidity and mortality in recent studies has been between 1% (Matjasko et al, 1985) and 7% (Millar, 1972). CONCLUSION The sitting position is safe, as shown by the low morbidity and mortality data, provided that care is taken to select the patients. Those with ischaemic heart disease, severe hypertension and known right-to-left intracardiac shunts are probably not suitable for operation in this position. Prophylaxis is paramount, by a combination of lower body compression augmented with intravenous fluids and PEEP, and adjusted to maximize the benefits to the right atrial pressure without spoiling the surgical field. Monitoring of the patient for venous air embolism should consist of a minimum of two devices, such as the Doppler and end tidal carbon dioxide, together with the ability to remove air via a right atrial catheter. The anaesthetist should be vigilant and have a low threshold of response to any changes that occur during the operation that may indicate an air embolism. REFERENCES Adornato DC, Gildenberg MD, Ferrario CM, Smart J & Frost EAM (1978) Pathophysiology of intravenous air embolism in dogs. Anesthesiology 49: 120-127. Albin MS (1984) The paradoxic air embolism--PEEP, Valsalva and patent foramen ovale. Should the sitting position be abandoned? Anesthesiology 61: 222-223. Albin MS, Jannetta PJ, Maroon JC, Tung A & MiUen JE (1974) Anesthesia in the sitting position. IV., European Congress of Anesthesiology, pp 775-778. Madrid: Excerpta Medica. Amsterdam. Albin MS, Babinski M, Maroon JC & Jannetta PJ (1976) Anesthetic management of posterior fossa surgery in the sitting position. Acta Anaesthesiologica Scandinavica 20: 117-128. Albin MS, Chang JL, Babinski M et al (1979) Intra-cardiac catheters in neurosurgical anesthesia. Anesthesiology 50: 67-68. Albin MS, Babinski MF, Gilbert J & Smith SL (1983) Venous air embolism is not restricted to neurosurgery! Anesthesiology 59: 151. Anderson KH (1983) Air aspirated from the venous system during total hip replacement. Anaesthesia 38: 1175-1178. Auer L (1976) Anti-Gravitationsanzug gegen akuten Blutdruckabfall bei Operationen in sitzender Lagerung. Acta Neurochirurgica 32: 131-137. Bedford RF, Marshall WK, Butler A & Welsh JE (1981) Cardiac catheters for diagnosis and treatment of venous air embolism. Journal of Neurosurgery 55: 610--614. Beloucif S, Raggueneau JL, Payen DM, George B & Echter E (1986) Beneficial effects on

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venous air embolism incidence of combined decreased systemic venous compliance (LBPP) and fluid loading. Anesthesiology 65: A363. Brechner VL & Bethune RWM (1971) Recent advances in monitoring pulmonary air embolism. Anesthesia and Analgesia Current Researches 50: 255-261. Buckland RW & Manners JM (1976) Venous air embolism during neurosurgery. Anaesthesia 31: 633-643. Bunegin L, Albin MS, Helsel PE, Hoffman A & Hung T-K (1981) Positioning the right atrial catheter. Anesthesiology 55: 343-348. Burton RR & Krutz RW (1975) G tolerance and protection with anti-G suit concepts. Aviation and Environmental Medicine 46: 119-124. Butler BD & Hills B A (1979) The lung as a filter for microbubbles. Journal of Applied Physiology 47: 537-543. Butler BD & Hills BA (1985) Transpulmonary passage of venous air emboli. Journal of Applied Physiology 59: 543-547. Butler BD, Bryan-Brown C & Hills BA (1983a) Paradoxical air embolism: transcapillary route. Critical Care Medicine 11: 837. Butler BD, Luehr S, Hills B & Katz J (1985b) Nitrous oxide anesthesia and pulmonary air embolism. Anesthesiology 63: A422. Butler BD, Leiman BC, Luehr S & Katz J (1986c) Effects of PEEP on the incidence of paradoxical air embolism in the absence of ASD in dogs. Anesthesiology 65: A81. Cabezudo JM, Gilsanz F, Vaquero J, Areitio E & Martinez R (1981) Air embolism from wounds from a pin-type head-holder as a complication of posterior fossa surgery in the sitting position. Journal of Neurosurgery 55: 147-148. Campkin TV (1981) Posture and ventilation during posterior fossa and cervical operations. British Journal of Anaesthesia 53: 881-883. Clayton DG, Evans P, Williams C & Thurlow AC (1985) Paradoxical air embolism during neurosurgery. Anaesthesia 40: 981-989. Colley PS & Artru A A (1984) ECG-guided placement of Sorenson CVP catheters. Anesthesia and Analgesia 63: 953-956. Colohan ART, Perkins NAK, Bedford RF & Jane JA (1985) Intravenous fluid loading as prophylaxis for paradoxical venous air embolism. Journal of Neurosurgery 62: 839-842. Crile GW (1909) Haemorrhage and Transfusion. Experimental and Research, pp 139. New York: D. Appleton & Co. Cucchiara RF (1984) Safety of sitting position. Anesthesiology 61: 790. Cucchiara RF, Nugent M, Seward J & Messick JM (1984) Detection of air embolism in upright neurosurgical patients by 2-D transesophageal echocardiography. Anesthesiology 60: 353-355. Dalrymple DG, MacGowan SW & Macleod GF (1979) Cardiorespiratory effects of the sitting position in neurosurgery. British Journal of Anaesthesia 51: 1079-1081. Durant TM, Long J & Oppenheimer MJ (1947) Pulmonary (venous) air embolism. American Heart Journal 33: 269-281. Edelman JD & Wingard DW (1980) Air embolism arising from burr holes. Anesthesiology 53: 167-168. Edmonds-Seal J, Prys-Roberts C & Adams AP (1971) Air embolism, a comparison of various methods of detection. Anaesthesia 26: 202-208. Edwards JE (1968) Interatrial communication. In Gould SE (ed.) Pathology of the Heart, pp 260-261. Illinois: Charles C Thomas. Ellis SC, Bryan-Brown CW & Hyderally H (1975) Massive swelling of the head and neck. Anesthesiology 42: 102-103. English JB, Westenskow D, Hodges MR & Stanley TH (1978) Comparison of venous air embolism monitoring methods in supine dogs. Anesthesiology 48: 425-429. Ericsson JA, Gottlieb JD & Sweet RB (1964) Closed chest massage in the treatment of venous air embolism. New England Journal of Medicine 270: 1353-1354. Fischler M, Vourc'h G, Dubourg O & Bourdarias JP (1984) Patent ovale and sitting position. Anesthesiology 60: 83. Freuchen IP (1959) The use of an anti-gravity suit in neurosurgery. Acta Anaesthesiologica Scandinavica 3: 17-23. Frost EAM (1984) Some inquiries in neuroanesthesia and neurological supportive care. Journal of Neurosurgery 60: 673-686.

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Furuya H, Suzuki T, Okumura F, Kishi Y & Uefuji T (1983) Detection of air embolism by transesophageal echocardiography. Anesthesiology 58: 126-131. Gardner WJ & Dohn DF (1956) The anti-gravity suit (G-suit) in surgery. Journal of the American Medical Association 162: 274-276. Geevarghese KP (1977) Anesthetic management of patients undergoing surgery for posterior fossa lesions. International Anesthesiology Clinics 15: 165-194. Gildenberg PL, O'Brien RP, Britt WJ & Frost EAM (1981) The efficacy of Doppler monitoring for the detection of venous air embolism. Journal of Neurosurgery 54: 75-78. Gilsanz FJ & Avello F (1982) PEEP and air embolism in the sitting position. British Journal of Anaesthesia 54: 110-111. Glenski JA, Cucchiara RF & Michenfelder JD (1986) Transesophageal echocardiography and transcutaneous Oz and CO2 monitoring for detection of venous air embolism. Anesthesiology 64: 541-545. Gronert GA, Messick JM, Cucchiara RF & Michenfelder JD (1979) Paradoxical air embolism from a patent foramen ovale. Anesthesiology 50: 548-549. Guggiari M, Lechat PH, Garen C, Darnat S & Viars P (1985) Prevention of paradoxical air embolism by 2-D contrast echocardiography in neurosurgical patients. Anesthesiology 63: A425. Hamby WB & Terry RN (1952) Air embolism in operations done in the sitting position. A report of 5 cases and one of rescue by a simple maneuver. Surgery 31: 212-215. Harris M, Yemen T, Stratford M e t al (1985) Venous air embolism during craniectomies in supine infants. Anesthesiology 63: A424. Hewer AJH & Logue V (1962) Methods of increasing the safety of neuroanaesthesia in the sitting position. Anaesthesia 17: 476-481. Hibino H & Matsuura M (1985) Cerebral venous sinus pressure in seated dogs: impact of PEEP, cervical venous compression and abdominal compression. Anesthesiology 63: 184-189. Higgins JR, Strunk BL & Schiller NB (1984) Diagnosis of paradoxical embolism with contrast echocardiography. American Heart Journal 107: 375-377. Ingrain GS & Brodrick PM (1986) The cardiovascular responses to the anti-gravity suit (G-suit) in sitting neurosurgical patients. In Bergmann H, Kramar H & Steinbereithner K (eds) Vllth European Congress ofAnaesthesiology, pp 179. Vienna: Verlag Wilhelm Maudrich. Ishak BA, Seleny FL & Noah ZL (1976) Venous air embolism, a possible cause of acute pulmonary oedema. Anesthesiology 45: 453-455. Katz J, Leiman BC, Luehr S & Butler BD (1986) Effects ofisoflurane on pulmonary filtration of venous air embolism in dogs. Anesthesiology 65: A362. Kitahata LM & Katz JD (1976) Tension pneumocephalus after posterior fossa craniotomy, a complication of the sitting position. Anesthesiology 44: 448-450. Lee DS, Lichtmann MW & Weintraub HD (1981) Effect of PEEP on air embolism during sitting neurosurgical procedures. Anesthesia and Analgesia 60: 262. Lee DS, Kuhn J, Shaffer MJ & Weintraub HD (1984) Migration of tips of CV catheters in seated patients. Anesthesia and Analgesia 63: 949-952. Leivers D, Spilsbury RA & Young JVI (1971) Air embolism during neurosurgery in the sitting position. British Journal of Anaesthesia 43: 84-89. Lewis JM & Rees GAD (1964) Electrocardiography during posterior fossa operations. British Journal of Anaesthesia 36: 63-64. Marquez J, Sladen A, Gendell H, Boehnke M & Mendelow H (1981) Paradoxical air embolism without intra-cardiac septal defect. Journal of Neurosurgery 55: 997-1000. Marshall BM (1965) Air embolus in neurosurgical anaesthesia, its diagnosis and treatment. Canadian Anaesthetist's Society Journal 12: 255-261. Marshall WK, Bedford RF & Miller ED (1983) Cardiovascular responses in the seated position--four anaesthetic techniques. Anesthesia and Analgesia 62: 648-653. Martin JT (1970a) Introduction and basic equipment (neuroanesthetic adjuncts for surgery in the sitting position: I). Anesthesia and Analgesia Current Researches 49: 576-587. Martin JT (1970b) The anti-gravity suit (neuroanesthetic adjuncts for surgery in the sitting position: II). Anesthesia and Analgesia Current Researches 49: 588-593. Martin JT (1970c) Intravascular electrocardiography. (Neuroanesthetic adjuncts for surgery in the sitting position: III). Anesthesia and Analgesia Current Researches 49: 793-808. Martin JT (1978) Positioning in Anesthesia and Surgery, pp 44-79. Philadelphia: WB Saunders.

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Martin RW & Colley PS (1983) Evaluation of transesophageal doppler detection of air embolism in dogs. Anesthesiology 58:117-123. Matjasko J, Petrozza P, Cohen M & Steinberg P (1985) Anesthesia and surgery in the seated position: analysis of 554 cases. Neurosurgery 17: 695-702. Mehta M & Sokoll MD (1981) Relation of right and left atrial pressure during venous air embolism. Anesthesiology 55: A238. Merrill DO, Samuels SI & Silverberg GD (1982) Venous air embolism of uncertain etiology. Anesthesia and Analgesia 61: 65-66. Michenfelder JD (1981) Central venous catheters in the management of air embolism: whether as well as where. Anesthesiology 55: 339-341. Michenfelder JD, Martin JT, Altenburg BM & Rehder K (1969) Air embolism during neurosurgery, evaluation of right atrial catheters for diagnosis and treatment. Journal of the American Medical Association 208: 1353-1358. Michenfelder JD, Miller RH & Gronert G A (1972) Evaluation of an ultrasonic device (Doppler) for the diagnosis of venous air embolism. Anesthesiology 36: 164-167. Millar RA (1972) Neuroanaesthesia in the sitting position. British Journal of Anaesthesia 44: 495-504. Mills NL & Ochsner JL (1980) Massive air embolism during cardiopulmonary bypass. Journal of Cardiovascular Surgery 80: 708-717. Munson ES (1971) Effect of nitrous oxide on the pulmonary circulation during venous air embolism. Anesthesia and Analgesia Current Researches 50: 785-792. Newfield P (1980) Anesthesia for posterior fossa procedures. In Cottrell JE & Turndorf H (eds) Anesthesia and Neurosurgery, pp 173-176. St Louis: Mosby. Nunn JF (1959) Controlled respiration in neurosurgical anaesthesia. Anaesthesia 14: 413-414. O'Higgins JW (1970) Air embolism during neurosurgery. British Journal of Anaesthesia 42: 459-462. Oliver S & Cucchiara R (1986) Comparison of outcome following posterior fossa craniotomy done in either a sitting or horizontal position. Anesthesiology 65: A305. Ordway CB (1974) Air embolus via CVP catheter without positive pressure. Annals of Surgery 179: 479-481. Pearl RG & Lawson CP (1986) Hemodynamic effects of PEEP during continuous venous air embolism in the dog. Anesthesiology 64: 724-729. Perkins NAK & Bedford RF (1984) Hemodynamic consequences of PEEP in seated neurological patients--implications for paradoxical air embolism. Anesthesia and Analgesia 63: 429-432. Perkins-Pearson NAK, Marshall WK & Bedford RF (1982) Atrial pressures in the seated position. Anesthesiology 57: 493-497. Pershau RA, Munson ES & Chapin JC (1976) Pulmonary interstitial oedema after multiple venous air emboli. Anesthesiology 45: 364-368. Pfitzner J & McLean A G (1985) Controlled neck compression in neurosurgery. Studies on venous air embolism in upright sheep. Anaesthesia 40: 624-629. Richardson HF, Coles BC & Hall GE (1937) Experimental gas embolism: I. Intravenous air embolism. Canadian Medical Association Journal 36: 584-588. Roewer N, Beck H, Kochs E et al (1985) Detection of venous embolism during intraoperative monitoring by 2-D transoesophageal echocardiography. Anesthesiology 63: A169. Sale JP (1984) Prevention of air embolism during sitting neurosurgery (the use of an inflatable neck tourniquet). Anaesthesia 39: 795-799. Sato S, Toya S, Ohira T, Mine T & Grieg NH (1986) Echocardiographic detection and treatment of intraoperative air embolism. Journal of Neurosurgery 64: 440-444. Senn N (1885) An experimental and clinical study of air embolism. Annals of Surgery 2: 197-313. Shapiro HM & Aidinis SJ (1975) Neurosurgical anesthesia. Surgical Clinics of North America 55: 919-920. Shapiro HM, Yoachim J & Marshall LF (1982) Nitrous oxide challenge for detection of residual intravascular pulmonary gas following venous air embolism. Anesthesia and Analgesia 61: 304-306. Shenkin HN & Goldfedder P (1969) Air embolism from exposure of the posterior cranial fossa in the prone position. Journal of the American Medical Association 210: 726.

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Sink JD, Comer PB, James PM & Loveland SR (1976) Evaluation of catheter placement in the treatment of venous air embolism. Annals of Surgery 183: 58-61. Sloan TB & Kimovec MA (1986) Detection of venous air embolism by airway pressure. Anesthesiology 64: 645-647. Standefer M, Bay JW & Trusso R (1984) The sitting position in neurosurgery: a retrospective analysis of 488 cases. Neurosurgery 14: 649-658. Steffey EP, Gauger GE & Eger EI (1974) Cardiovascular effects of venous air embolism during air and oxygen breathing. Anesthesia and Analgesia 53: 599-604. Symons NLP & Leaver HL (1985) Air embolism during craniotomy in the seated position: a comparison of methods of detection. Canadian Anaesthetist's Society Journal 32: 174--177. Tateishi H (1972) Prospective study of air embolism. British Journal of Anaesthesia 44: 1306-1310. Tattersall MP (1984) Complications of the sitting position: massive swelling of the face and tongue. Anaesthesia 39: 1015-1017. Tausk HC & Miller R (1983) Anesthesia for posterior fossa surgery in the sitting position. Bulletin of the New York Academy of Medicine 59: 771-783. Tindall GT, Craddock A & Greenfield JC (1967) Effects of sitting position on blood flow in the internal carotid artery. Journal of Neurosurgery 26: 383. Tinker JH & Vandam LD (1972) The O Suit, How effective is it in neurosurgical operations. Anesthesiology 36: 609-611. Tinker JH, Gronert GA, Messick JM & Michenfelder JD (1975) Detection of air embolism, a test for positioning of right atrial catheter and doppler probe. Anesthesiology 43: 104--106. Toung TJK, Alano J & Nagel EL (1980) Effects of MAST suit on central venous pressure in the sitting position. Anesthesiology 53: $188. Toung T, Ngeow YK, Long DL, Rogers MC & Traystman RJ (1984) Comparison of the effects of PEEP and jugular venous compression on canine cerebral venous pressure. Anesthesiology 61: 169-172. Tuman KJ, Spiess BD, McCarthy RJ & Ivanovich AD (1986) Cardiorespiratory effects of venous air embolism in dogs receiving a perfluorocarbon emulsion. Journal of Neurosurgery 65: 238-244. Voorhies RM, Fraser A R & Poznak AV (1983) Prevention of air embolism with positive and expiratory pressure. Neurosurgery 12: 503-506. Ward RJ, Danziger F, Bonica JJ, Allen GD & Tolas AG (1966) The cardiovascular effects of change in posture. Aerospace Medicine 37: 257-259. Wolffe JB & Robertson HF (1935) Experimental air embolism. Annals of Internal Medicine 9: 162-165. Wood EH & Lambert EH (1952) Some factors which influence protection afforded by pneumatic anti-gravity suits. Journal of Aviation Medicine 23: 218. Young ML, Smith DS, Murtagh F, Vasquez A & Levitt J (1986) Comparison of surgical and anesthetic complications in neurosurgical patients experiencing venous air embolism in the sitting position. Neurosurgery 18: 157-161. Zasslow MA, Pearl PG, Lawson CP & Silverberg G (1986) PEEP does not affect left atrial-right atrial pressure gradient in neurosurgical patients. Anesthesiology 65: A304.