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Clinical Reports Fatal air embolism during dental implant surgery: a report of three cases Between October 6, 1986 and September 17, 1987, 11 patients underwent insertion of mandibular dental prostheses by the same oral surgeon. Three patients suffered cardiac arrest during surgery and subsequently died. Two of the patients who died had received general anaesthetics and the other had intravenous sedation given by three different anaesthetists. All three patients arrested suddenly, developing profound cyanosis and electrical mechanical dissociation, underwent prolonged resuscitative efforts, and had marked hypoxaemia and hypercapnia, despite cardiopulmonary resuscitation. Two other patients had signs of injection of air but survived, one suffering cardiac collapse and the other sustaining massive subcutaneous emphysema. Air embolism was produced by inadvertent injection of a mixture of air and water, passing through the hollow dental drill, directly into the mandible to the facial and pterygoid plexus veins and thence to the superior vena cava and right atrium. Du 6 octobre 1986 au 17 septembre 1987, le mdme chirurgiendentiste procdda d l'insertion intramandibulaire de proth~ses chez 11 patients. Trois d'entre eux succomb~rent d un arr~t cardiaque pendant l' intervention. Trois anesthdsistes diffdrents avaient utilisd dans deux cas, une anesthdsie gdnerale et dans l'autre, de la sddation par voie intraveineuse. La dissociation

Key words ANAESTHESIA: dental; COMPLICATIONS:death, embolism, morbidity; EMBOLISM: air; SURGERY: dental.

From the *Department of Anaesthesia, Foothills Hospital at the University of Calgary, Calgary, Alberta. and tMedical Investigations, Office of the Chief Coroner of British Columbia, Burnaby, British Columbia. Address correspondence to: Dr. J.M. Davies, Department of Anaesthesia, Foothills Hospital at the University of Calgary, 1403 - 29th St. N.W., Calgary, Alberta, Canada T2N 2T9. CAN ] ANAESTH 1990 / 3 7 : 1 /pp112-21

J.M. Davies MScMDFRCPC,* Linda A. Campbell RNt

dlectro-mdcanique doublde de cyanose survenait brutalement et demeurait rdfractaire aux efforts prolongds de rdanimation avec hypoxdmie et hypercarbie marquds. Une emphysdme souscutand spectaculaire chez Fun et un dpisode de collapsus cardiovasculaire chez I'autre, fit suspecter une injection d'air chez deux survivants. Il s'avdra qu'un mdlange accidentel d'air et d' eau irriguant la fraise dentaire se trouvait injectd directement dans le maxillaire infdrieur, et de hi, par les plexus veineux faciaux et ptdrygofdiens allait jusqu'd la veine cave et ti l' oreillette droite, crdant une embolie adrienne massive.

Dental implants to replace dentures have been in use for about 18 years. Since 1984, more than 80,000 implants have been placed in American patients, 120,000 in patients worldwide. The Interpore IMZ System was developed in Europe in the 1970's. More than 25,000 of these have been placed in American and European patients.* The implant technique requires that a precise hole be cut in the jaw, into which a titanium cylinder is sunk. To the top of the cylinder, which is level with the gum, is affixed a single tooth. If more teeth are required, as with a denture, then a second cylinder is implanted. Surgery is performed in two stages: insertion of the cylinder and placement of the tooth/teeth. The first stage consists of four major steps, during each of which either external (around the drill bit onto the bone) or internal (through the drill bit into the bone) irrigation is used. This liquid clears away debris produced during the procedure and cools the drill bit and bone, so that bone temperature does not exceed 43 ~ C and cause death of bone cells. For external irrigation, liquid or liquid/air may be used; for internal irrigation the Interpore IMZ Technique Manual describes the use of "sterile normal saline solution."* Thus, to place the cylinder, the cortical bone is marked through a perforated template and through the jaw mucosa *Interpore International, Dental Implantology Fact Sheet, Irvine, California.

Davies and Campbell: DENTAL AIR EMBOLISM with the externally irrigated spiral drill. After elevation of the mucoperiosteal flaps, a 2.0 mm diameter pilot hole is drilled, using the hollow drill with "copious irrigation."* The IMZ Manual emphasizes the importance of confirming "saline flow through ... the drill prior to starting the drilling procedure." Then the pilot hole is enlarged and countersunk, using a round drill with external irrigation. Finally, the implant site is enlarged to a depth of 13 mm using in sequence "internally irrigated 2.8 mm, 3.3 mm, and 4.0 m m . . . cannon drills."* The cylinder is then fixed into the hole and the incision closed. Five case reports are presented, not in chronological order, but in the sequence by which they came to public attention.

Case reports Patient 1 On June 19, 1987, a 16-year-old, 80 kg white male presented to Dental Office A for stage one implant surgery to replace two left mandibular teeth. Past medical history revealed pneumonia twice as an infant and an undocumented allergy to procaine (Novocain). He had had two uneventful general anaesthetics, the most recent 14 months previously. Preoperative physical examination revealed no abnormality although he was very nervous. The patient was classified as ASA physical status I. General anaesthesia was induced by anaesthetist #1 with injection into the right antecubital fossa vein of a combination of methohexitone 80 mg, atropine 0.6 mg, gallamine 20 mg and succinylcholine 80 mg. Drugs were injected through intravenous access established in a vein on the dorsum of the right hand (but not maintained during the procedure). Left nasal intubation was accomplished, the cords were visualized with a laryngoscope, and passage of the uncuffed tube through them observed. The anaesthetist auscultated the chest to confirm placement of the tube in the trachea. The anaesthetic was continued with two per cent halothane, which was raised briefly to three per cent and then decreased to 0.5 per cent, and a 50/50 mixture of nitrous oxide-oxygen at 4 L. min -t through a circle system. The patient resumed spontaneous ventilation about five minutes after anaesthesia was induced. A pulse meter attached to a right-hand finger (the only monitor used) showed the heart rate to be 100-120 beats, min -I and regular. The surgeon inserted a throat pack and then injected one carpule (1.7 ml) of articaine HCL four per cent with epinephrine 1/200,000 (ultracaine DS). He reflected a full thickness mucoperiosteal flap from the left edentulous

*Interpore International, Dental Implantology Fact Sheet, Irvine, California.

1 13 mandibuloalveolar ridge and noted that the blood was "pink." He then drilled an initial 2.0 mm intra-osseous hole, but expressed frustration at the function of the drill. The patient continued to breathe spontaneously. About 25 minutes after induction of anaesthesia, the surgeon was drilling the second hole (at the 2.8 mm stage) when he noted pallor of the oral and facial tissue. The pulse meter slowed. Seconds later he observed darkening of blood in the wound and dusky facies that were "purply blotchy." He placed a gauze pad over the wound. The drapes were removed from the patient's neck and chest which was noted to be pale and cyanosed. The nurse observed that the face was "very cyanotic." The anaesthetist was unable to feel a good radial pulse and therefore palpated the carotids. He then auscultated the chest; the heart rate was thought to be 60 beats, min-~ and bilateral air entry was heard. He discontinued the nitrous oxide and the halothane and administered 100 per cent oxygen. He again auscultated the chest and thought the heart rate to be 40 beats, min -~. The patient's respiratory rate decreased and the anaesthetist assisted ventilation. Atropine 0.6 mg was given through the left external jugular vein. The anaesthetist administered a precordial thump and started cardiopulmonary resuscitation (CPR). Paramedics were called. Epinephrine 0.1 ml of 1/1000 was given, then 50 ml of 8.4 per cent sodium bicarbonate, through the left external jugular vein. Three separate injections were made into the vein. An attempt was made to defibrillate, but the machine was not working, in either the plugged or unplugged state. Paramedics arrived. The patient was transported to the local hospital about ten minutes after arresting. During transport, a paramedic auscultated the patient's chest and heard bilateral air entry and none at the abdomen and was assured that the tracheal tube was properly placed. Two-man CPR was continued during transport to the hospital. At the hospital, monitors were attached and an intravenous line started. The patient was noted to be "blue from the nipple line up." The chest rose with each respiration, air entry was heard equally bilaterally and there was no bronchospasm. The monitor showed the occasional QRS complex: however, there was no cardiac output with this activity. Despite continued CPR, replacement of the tracheal tube twice, and a transvenous pacemaker, electrical mechanical dissociation (EMD) and profound peripheral and central cyanosis persisted. The cyanosis was most evident over the upper body. Subcutaneous emphysema was noted over the left neck and anterior chest wall. A second intravenous line was established in the left arm. A blood gas sample from the right femoral artery showed a pH of 7.31, PCO2 64 mmHg, PO2 19 mmHg, a base excess of 2.6 mEq. L -l , and an oxygen saturation of 2.4

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per cent. Repeat arterial blood gas sampling showed a pH of 7.39, PCO2 72 mmHg, PO2 14 mmHg, a base excess of 4.5 mEq. L- i, and an oxygen saturation of 17 per cent. A portable chest x-ray revealed "diffuse subcutaneous emphysema in the neck, particularly on the left." There was a diffuse alveolar pattern consistent with pulmonary oedema. An arterial line was placed in the right radial artery and blood gas sampling showed improvement in blood gas values, with a pH of 7.48, PCO2 34 mmHg, PO2 74 mmHg, a base excess of 2.7 mEq .L -1, and an oxygen saturation of 96 per cent. After pacemaker insertion and dopamine infusion, a systolic blood pressure of 58 mmHg was detected but CPR was required to maintain an output. After 62 minutes of resuscitation in hospital and discussion among the attending staff physicians, the dopamine was discontinued. The patient had no blood pressure nor cardiac output, nor audible cardiac sounds despite electrical activity. His pupils were fixed and dilated. He had absent corneal reflexes, a negative doll's head reflex, and no response to caloric testing. The patient was pronounced dead, 83 minutes after suffering cardiac arrest. Autopsy, performed two hours later, showed subcutaneous emphysema of the neck and left supraclavicular area from the midline to the acromion. The tracheal tube was correctly placed and not obstructed. Both lungs had areas of focal atelectasis. The left lung was slightly to moderately crepitant. A gauze was found in the oesophagus. The brain grossly showed evidence of oedema (obliteration of convexity sulci, tonsillar herniation, and narrowing of the ventricular system). Patient 2 On November 6, 1986 a 50-year-old, 88 kg white male presented to Dental Office B for stage one implant surgery to replace a complete mandibular denture. He had a history of anicteric infectious hepatitis 18 years previously, moderate alcohol intake associated with mildly abnormal liver function tests one year before, and treatment with an antidepressant and an anxiolytic that same year. Testing for hepatitis A and B (in 1985) was negative. Two weeks before surgery his only complaint was of arthritis; he had not taken any medication for several months. He denied any problems with general anaesthetics. General anaesthesia was induced by anaesthetist # 2 by direct intravenous injection of methohexitone 190 mg, gallamine 20 mg and succinylcholine 80 mg. Ventilation by mask with 100 per cent oxygen and three per cent halothane was performed for 30 seconds and then right nasotracheal intubation accomplished with an uncuffed 7.5 mm tube, Anaesthesia was maintained with nitrous oxide 7 L. min -1 and oxygen 5 L. min -1, through a circle system, and two per cent halothane which was then

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decreased to 1.5 per cent. Spontaneous ventilation resumed after about three minutes. No monitors were used. The surgeon performed bilateral mandibular nerve blocks plus anterior infiltration with three carpules (1.8 ml each) ofmepivacaine two per cent with levonordefrine 1/20,000 (Citanest Forte). A full thickness flap was reflected from the left anterior mandibular ridge. Forty minutes after induction of anaesthesia, the hole for the second implant was being prepared when the patient appeared to move slightly. The anaesthetist resumed control of ventilation. The patient then exhibited "seizure-like activity," and was thought to be light. The concentration of halothane was increased to two per cent and ventilation assisted. The patient's colour was then noted to be less than optimal, with desaturation occurring within 30 seconds after the increased halothane concentration and assisted ventilation. Because of "mild cyanosis" and absence of a palpable pulse, the position of the tracheal tube was checked. The anaesthetic was discontinued and the patient tilted head down. Oxygen was administered and the patient's lungs were hyperventilated, but despite this and external cardiac massage there was no improvement in the patient's condition. Fourteen minutes after the patient arrested, paramedics were called and arrived within two minutes. Electrocardiographic monitoring was established by the paramedics who also attempted to obtain intravenous access in both antecubital fossa and the left external jugular vein (twice), but without success. The patient's trachea was reintubated with a cuffed 8.0 mm tracheal tube and epinephrine and atropine given through it. During this time the monitor showed EMD until 16 minutes after the paramedics arrived when second degree A-V block at 75 beats, min- 1with output was observed. Paramedics transported the patient to the local hospital. The patient's pupils were fixed and dilated. He was comatose and cyanosed, without respiratory efforts, and with a faint, weak and intermittent pulse. Forty-four minutes after arresting, the patient's jugular venous pressure was markedly elevated. An electrocardiograph (ECG) trace showed a ventricular rate of 44 beats, min- 1 with right bundle branch block, third degree A-V block, and elevated ST segments compatible with acute anterior and inferior injury. Arterial blood gas sampling showed a pH of 7.41, PCO2 70 mmHg, PO2 56 mmHg, and a base excess of 15 mEq .L -t. A dopamine infusion was started and the blood pressure increased from 40/0 mmHg to 98/60 mmHg, with a heart rate of 57 beats, min- 1. Repeat arterial blood gas sampling showed apH of 7.18, PCO2 50 mmHg, PO2 70 mmHg, and a base deficit of 10 mEq. L -l. After an episode of ventricular tachycardia, treated with defibrillation and lidocaine, the

Davies and Campbell: DENTAL AIR EMBOLISM blood pressure increased to 120/70 mmHg. A temporary pacemaker was inserted and mechanical ventilation instituted. A chest x-ray showed interstitial and early alveolar oedema, with prominent pulmonary arteries, bronchial cuffing, and redistribution of pulmonary vessels. The patient's neurological status was assessed and prognosis thought to be poor. Over the next two days the patient developed progressive cardiac failure. It was determined that he had irreversible cerebral damage and was declared dead three days after the cardiac arrest. Autopsy performed the next day showed acute purulent bronchitis and early bronchopneumonia. The liver was enlarged with severe fatty changes involving virtually all the liver cells. Although there were no areas of critical narrowing of the coronary vessels nor occlusive thrombi, there was extensive recent infarction of the posterior and inferior walls of both ventricles and the posterior portion of the interventricular septum. This extended to the lateral free-wall of the right ventricle. Both ventricular chambers were acutely dilated. The pathologist added the comment that the deceased "appeared to have suffered an episode of coronary artery spasm while under anesthesia." In addition, there was ischaemic brain injury. Patient 3

On September 17, 1987 a 48-year-old, 64 kg white female presented to Dental Office B for implant surgery to replace a complete mandibular denture. She had a four-year history of multiple complaints compatible with a diagnosis of lupus erythematosus. Episodes of chest pain one year previously had initially been ascribed to myocardial ischaemia; however, thallium scanning was normal and a diagnosis of chest wall syndrome was made. She took only premarin and was allergic to ASA. She had had previous anaesthetics without problems. On the day of surgery, ampicillin 500 mg was given orally. The surgeon assessed her as being extremely nervous. Intravenous sedation was given by anaesthetist # 3 in the form of diazepam 10 mg and methohexitone 70 mg. These were administered in intermittent doses, with most of the drugs given in the first 15-20 minutes. Drugs were given through intravenous access established in a left ann vein and kept patent by an infusion of five per cent dextrose in water. The surgeon performed bilateral mandibular nerve blocks plus local infiltration. He used three carpules (1.8 ml each) of mepivacaine two per cent with levonordefrine 1/20,000 (Citanest Forte) after the first increments of intravenous medications had been given. The patient's heart rate was 80-90 beats, min -~, determined by the anaesthetist who intermittently palpated the patient's radial pulse. No other monitor was used. A full thickness flap was developed on the left mandibular

115 ridge, the hole drilled, and the implant inserted. The surgeon then asked the patient to turn her head, which she did. The anaesthetist did not notice anything unusual except that the hand-piece of the drill was leaking water. About 50 minutes after the start of the procedure, the surgeon made a full thickness flap on the right anterior mandibular ridge. He then started to drill the second implant site. The patient complained of pain. The surgeon asked, "Where?" and the patient responded "In the mouth." He then injected one more carpule of mepivacaine and started drilling again. The anaesthetist injected methohexitone l 0 mg. The bite block was noted to slip out of position. Seconds later, the patient coughed, jerked, became cyanotic and had no pulse or respirations. The anaesthetist placed her in the head-down position, inserted an oral airway, and ventilated her with 100 per cent oxygen by mask. There was no improvement in her colour and her pupils were widely dilated. An uncuffed tracheal tube and a throat pack were inserted. Electrocardiograph leads were placed and showed a very slow heart rate which then deteriorated into ventricular fibrillation. She was defibrillated and isoproterenol 3 ml of 1/5000 was given intravenously. The ECG showed an improvement in rhythm: the heart rate increased but then slowed and reverted to ventricular fibrillation. No pulse could be felt. The surgeon started external cardiac massage. Paramedics were called 15 minutes after the arrest and arrived at the dental office during the second defibrillation, which produced ventricular tachycardia for five seconds, then EMD at 80 beats, min -~. The paramedics resumed CPR. There was no detectable blood pressure or pulse. Despite ventilation, chest compression, and defibrillation, there was no change in the patient's colour, nor any effort to breathe spontaneously. Her pupils were widely dilated. A second intravenous line was established and a bolus injection of 500 ml of normal saline given by the paramedics. After 39 minutes of (advanced) cardiac life support, the paramedic team left the office with the patient. She continued to have EMD with supraventricular tachycardia, although a pressure of 50/? mmHg was recorded just before arrival at the hospital. There the patient had a palpable pulse with an irregular rate of 75-100 beats, rain -~. The CPR was discontinued and a dopamine infusion started, raising the blood pressure to 105 mmHg systolic. Venous pressures in the neck were only slightly increased. Air entry was heard equally over both sides of the thorax. No respiratory effort was noted. An arterial blood gas sample showed a pH of 6.9, PCO2 75 mmHg, POE 74 mmHg, a base deficit of 21 mEq. L -I, and an oxygen saturation of 78 per cent. An ECG showed right bundle branch block, with depressed ST segments in leads II, HI, AVF and V 1-6. A chest x-ray

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showed pulmonary oedema. She was assessed as having a Glasgow Coma Scale Score of 3/15. Twenty hours after suffering a cardiac arrest she was determined to have no cerebral function. Nine hours later she developed asystole. An autopsy performed three days later showed generalized swelling of the brain with bilateral hippocampal herniation and marked herniation of the cerebellar tonsils. There was a mild degree of atherosclerotic heart disease with no areas of greater than 25 per cent narrowing by plaque in any of the surface coronary vessels. Widespread contraction band necrosis was found. Death was determined to be due to "irreversible cerebral anoxic changes and diffuse myocardial necrosis due to prolonged cardiac arrest. There was, at autopsy, no evidence of a structural reason for this arrest in the form of a pre-existing disease condition ... The history indicates that at the time of her fatal collapse this woman was undergoing a dental procedure under general anesthesia. It is well established that sudden collapse and death can occur under such circumstances." Patient 4

On May 1, 1987 a 39-year-old, 82 kg white male presented to Dental Office A for mandibular implant surgery to replace a complete set of lower teeth that had been absent for at least 15 years. When he awoke from the general anaesthetic he noted that he had massive subcutaneous emphysema which extended from both nipples up to the cheekbones and swelling shut the left eye. This persisted for a week. Patient 5

On October 20, 1986 a 58-year-old, 60 kg white male presented to Dental Office B for bilateral mandibular implant surgery to replace a complete lower denture. He received local anaesthesia, without any sedation. Fifty minutes later the second implant hole had been drilled to 15 mm when the patient suddenly lost consciousness and became cyanotic. He had no palpable pulse or blood pressure but continued to breathe. Oxygen by mask and 50 mg diphenhydramine intravenously were given. He was placed in the head-down position. Forty-five minutes later the paramedics were called and the patient regained consciousness as one of the paramedics started an intravenous infusion in a forearm. He was assessed at the local hospital where an ECG (but no chest x-ray) was done. The ECG showed only "minor T changes" and was considered normal. He was discharged a few hours later. Diseussion Why did three patients die and two others suffer major complications during the course of the same surgical

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procedure? Three possibilities include hypoxia, drug- and hypercapnia-induced dysrhythmia, and surgical emphysema. The fourth, and most logical, explanation is that those who died suffered massive venous air embolism. The first possibility is tlaat the patients arrested because of hypoxia. Patients I and 2 received general anaesthetics typical of those used foi outpatient dental surgery, with reasonable drug doses. Although nitrous oxide/oxygen/ halothane with spontaneous ventilation is acceptable, it is safer when monitoring of oxygenation, pulse oximetry, is used. Unfortunately, in none of the cases was anything more than a pulsemeter employed. Neither patient was preoxygenated before tracheal intubation was performed. Patient 1 arrested 25 minutes and 2 at 30 minutes after induction of anaesthesia, thus excluding death as a complication of oesophageal intubation. Patients 1 and 2 were anaesthetized by different anaesthetists using different anaesthetic machines. The machine used for Patient 1 was inspected and found to have multiple defects. However, Patient 1 was the second case of the day, preceded by a young woman who underwent a 20-minute general anaesthetic, of similar technique and lack of monitoring, and who recovered uneventfully. Similarly, Patient 2 was the third case of the day. Patient 3 underwent intravenous sedation with a combination of drugs which could have depressed her ventilatory drive, resulting in hypoxia and hypercapnia. However, most of the drugs were given in the first 15 minutes and she arrested one hour after the start of the anaesthetic. Also, just before she arrested she was given a supplemental intravenous injection of methohexitone, but only 10 mg, which would be unlikely to produce marked respiratory depression in a middle-aged woman who weighed 64 kg. Furthermore, just before she arrested, the patient was awake enough to turn her head on command and then to complain of pain in her mouth when the surgeon started to drill the second implant site. Patient 5 had received local anaesthesia only and therefore should not have been hypoxic. A second possibility is that the patients developed a dysrhythmia. The three patients who died were reported by the surgeon to be very nervous preoperatively. Two underwent halothane anaesthetics with spontaneous ventilation and all patients received either epinephrine or neocobefrine mixed with the local anaesthetic. Thus it is possible that all who collapsed suffered some type of catecholamine-induced dysrhythmia, compounded by hypercapnia as a result of hypoventilation. Unfortunately, during surgery, neither electrocardiographic nor blood pressure monitoring was undertaken, and the anaesthetic record consisted only of a list of drugs and doses and a summary of events. It is therefore impossible to state exactly what happened before the patients collapsed.

Davies and Campbell: DENTAL AIR EMBOLISM However, it is highly improbable that four patients under the care of the same surgeon and three different anaesthetists would all succumb to a similar drug-induced problem. The doses used and the timing of drug administration would weigh against such a reaction. Furthermore, Patient 1 was only 16 years old and at autopsy did not have any evidence of pre-existing cardiac problems. Although a dysrhythmia could have been triggered, it should have been possible to resuscitate him and restore a normal rhythm more easily than occurred. Even though hypoxia or a dysrhythmia may (not) have been the cause of the problems, the presence of subcutaneous emphysema must still be explained. Thus, the third theory which must be considered is that the subcutaneous air found in three of the patients developed during anaesthesia, surgery or resuscitation. One possibility is that positive pressure ventilation forced air through the incision into the subcutaneous tissues of the neck. Patients 1 and 2 had undergone nasotracheal intubation. It is possible that in both cases laceration of the oral pharyngeal mucosa occurred during intubation, before placement of the throat pack. However, to postulate this would require that three different anaesthetists produced the same traumatic injury (to Patients 1,2 and 4), that Patients 1 and 2 died of independent causes, and that Patient 4's subcutaneous emphysema was entirely unrelated. Furthermore, this line of reasoning would require that subcutaneous emphysema after nasotracheal intubation be a common complication. We found only four reports of subcutaneous air not related to the surgical process. Smith et al. described two cases of a complication of traumatic tracheal intubation. One patient died. The authors went on to demonstrate that oxygen at 30 mmHg could be forced through a small (0.95 cm) incision in the mucosa of the pyriform sinus, t Scott and Viner reported two cases in children after difficult intubation. They suggested that use of an introducer with the tracheal tube would increase the likelihood of air being driven into the tissues.2 Golding et al. described the same complication, but after laceration of the pharynx during attempted passage of a nasogastric tube. Problems did not occur until three and one half hours postoperatively in the recovery room when dyspnoea developed. Administration of nasal oxygen was thought to have been the source of the gas in the tissues. 3 Finally, Jumper et al. reported pulmonary barotrauma from a faulty resuscitation bag used to ventilate the lungs of a patient by hand during transport from the operating room to recovery area. The patient, who had restrictive lung disease, developed subcutaneous emphysema without evidence of pneumothorax, and died 30 minutes later. Massive air mediastinitis was suspected. 4 However, in none of the patients reported here was there any indication of problems with intubation.

117 Thus is it unlikely that traumatic intubation and positive pressure ventilation (before placement of the throat pack) was the cause of the subcutaneous emphysema in the three patients. Patient 3 was the only one likely to have suffered that complication as, at the time of arrest, her lungs were ventilated by bag and mask before tracheal intubation. No air was noted in her tissues. Patients I and 2 had subcutaneous air in their left nuchal tissues and both had received injections and attempts at placement of intravenous access lines into the left external jugular vein. Theoretically, a needle tip could have entered the lung, causing an air leak with resultant emphysema. This would be more likely ifa line was left in the neck. Furthermore, no pleural air was seen on chest x-ray and no damage to the left lungs seen at autopsy. This rare occurrence would have to have been produced by two different anaesthetists. In addition, Patient 4 did not receive any resuscitative efforts, yet awoke from his general anaesthetic with massive soft tissue swelling. Numerous references describe subcutaneous emphysema as a complication of dental surgery.5-28 The cause may be due to an action of the patient in the postoperative period, such as blowing the nose, s coughing, 6 bugling, 7 or blowing up balloons. 8 Difficult or prolonged extractions also contribute. 9 "Idiopathic" appearance of air is rare. 1~ Irrigation with hydrogen peroxide tl may also produce excess oral gas, especially within tissue spaces. Most commonly, compressed air was used, either to power a high-speed drill or to irrigate the surgical site. 12-23As Bavinger stated, increased use of compressed air devices since the 1960's paralleled the "surge of reports in the literature of complications from their u s e . ,,24

For subcutaneous air to be produced, there must be both increased oropharyngeal pressure and a disruption of the oropharyngeal tissue. 9 "Air may enter the soft tissues either directly by being forced down the gingival crevice, or indirectly by being forced down a root canal and leaving by way of a perforation in the covering alveolar bone.'2~ Air then follows a superficial track, entering the buccal surface of the mandible, beneath the periosteum over the lower border where the facial vessels cross, down the neck (mainly near the anterior border of the sternocleidomastoid muscle), along the middle of the pretracheal layer, and then further down into the pectoral region, io,23 If the patient is in a head-up position, then air will also track up under the cheek to the lower eyelid and temporal region, i i The air may track "as far down the thorax as the sixth rib ''tl (about the "I'4dermatome), and as far up as the "top of the head, ''~ t as occurred to Patient 4. The only factors common to all patients were the position in the dental chair, the surgeon, the procedure, and the implant equipment. Although the theories of

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hypoxia, catecholamine-induced dysrhythmia, and emphysema produced during anaesthesia, surgery or resuscitation might be possibilities in an isolated case, only the occurrence of air embolism links the five patients. In addition, the five patients reported here represented 45 per cent of those on whom the surgeon had undertaken the implant procedure. Thus, an event common to all patients is required to explain the extremely high morbidity and mortality. For air embolism to occur there must be an open vessel, a gradient between extravascular and intravascular pressure, and a source of air. Bone tissue is very vascular; indeed, injection of catecholamines into the peridontal ligament is virtually the same as direct intravenous injection.29 The intraosseous venous plexus in the mandible gives rise to large veins in the interdental septum. These vessels are open sinuses in the bone; the walls are therefore rigid and unable to collapse when venous pressure decreases. The septal veins form several inferior alveolar veins, some of which flow through the anterior dental foramen to the facial vein, and others which flow through the inferior dental foramen to the pterygoid plexus. Both the facial vein and pterygoid plexus drain into the jugular vein. Risk of embolism increases when the pressure of the air, extravascular, is greater than the venous pressure, intravascular. The difference between these two pressures is the venous gradient, which may be due to gravity, causing a low or subatmospheric intravascular pressure, or to a forced source of air, causing a high extravascular pressure. Venous air embolism can occur with a gravitational gradient as low as 5 cm through tissue well supplied with veins or venous sinuses. 3~ All the patients were positioned in the dental chair at the same angle: about 20 ~ head up, flexed 10~ at the hips, creating a gradient of at least 15 cm between the lower jaw and the right atrium. In addition, all patients were fasting (presumably from midnight) and thus, all had intravascular volume depletion. Neither patient who received a general anaesthetic had any intravenous fluid replacement and those who died were given drugs which produce venous dilatation, resulting in further lowering of their venous pressures. Of the four patients who suffered cardiovascular collapse, all were breathing spontaneously. This results in a lower mean intrathoracic pressure than does controlled ventilation. Increased negative intrathoracic pressure may also result from spontaneous ventilation with a partially obstructed upper airway, 3~ as could have occurred with three of the patients. Furthermore, should surgical stimulation increase in a patient breathing spontaneously during general anaesthesia, the patient will respond by increasing rate and depth of ventilation. This may occur suddenly, as a gasp, with resultant marked increase in negative

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intrathoracic pressure. Such a gasp enhances entrainment of air into the venous system. A similar response might be seen with a patient who had received only local anaesthesia and sedation, as had Patient 3. Sudden stimulation of an incompletely anaesthetised area would have caused her to complain of pain in the mouth, and probably also to gasp, in response to the sensation of the drill in the second implant site. To perform the implant surgery, the surgeon used a KaVo dental handpiece, consisting of three parts: motor, shank and head (into which drill bits were inserted). The motor (INTRAmatic L-motor #181H) was designed for general dental use, including dental hygiene. It was driven by compressed air, which ran from tanks in the basement of both dental offices to a "doctor's cart." From the cart, the air passed to the base of the motor through one channel of a multi-lumen hose. After driving the motor, this air then returned down a separate lumen of the hose to the cart where it was exhausted into room air. Testing of the motor by the Standards and Testing Bureau of Radiation and Medical Devices, Ottawa, did not reveal any connection between the compressed air and the rest of the drill apparatus. Thus the motor was not the source of air embolism. If the handpiece had been purchased as part of an implant kit, then the shank's structure would have been different from the one purchased by the surgeon. With a kit handpiece, the only way of performing internal irrigation is by means of an accessory source of sterile coolant (e.g., from an intravenous bag and drip line), attached to the head of the implant equipment. However, the surgeon purchased the three components of the handpiece as separate items. The shank purchased (#29A) incorporated an external tubing system. This allowed liquid or air/liquid (from the multi-lumen hose attached to the base of the motor) to pass to the drill bits in the head. When supplied as a kit, the external tubing system is capped off by an external stainless steel sleeve. The implant manual describes the use of "sterile normal saline" for irrigation, which precludes the mixing of air and fluid. Despite this, the surgeon chose to use the coolant tap water delivered through the multi-lumen hose from the doctor's cart. In both Dental Offices A and B, coolant air was delivered with the water to the hand-piece. In Dental Office A, the coolant air pressure was 52-60 psi and in Office B was 36 psi (measured at the hand-piece). With a water flow of 50 ml-min - l , air flows of 2.5-5 L. min-l could be produced, with a pressure at the outlet of the drill bit of 80 cm H20. The patient's venous pressure of 10-15 cm H20 would be easily overcome by the jet of air/water emerging from the hollow drill bit. Furthermore, during surgery on Patients 1 and 3, the hand-piece was noted to be leaking water. With a constant

Davies and Campbell: DENTAL AIR EMBOLISM air and water pressure, if a mixture of air and water was delivered to the hand-piece and some of the water leaked from the hand-piece, then possibly even more air could be delivered to the patient. Thus, the combination of the use of equipment allowing passage of coolant from the doctor's cart plus the use of tap water from the cart as the irrigant was a fatal one. Not only does air embolism explain the cause of the collapse and of the subcutaneous air in these patients, it also explains the timing of the collapse and the resultant pathophysiology. All four patients who collapsed had undergone surgery to the same stage, i.e., completion of the first implant hole and drilling of the second hole started. All patients suddenly developed problems. This was more than the sudden observation by an anaesthetist of slowly developing problems in a poorly monitored patient, because it was seen simultaneously by the surgeon, dental assistant and anaesthetist (except with Patient 5 - no anaesthetist present). In 1937, Richardson and co-workers demonstrated that when injecting air at a rate of less than I ml. kg- i. min- 1, "fairly large quantities could be tolerated.'32 Butler and Hills later described the concept of a "critical" rate of infusion of air. 33 At rates less than 0.30 m l . k g - l . m i n -1, venous emboli were trapped in the pulmonary vasculature. Increased infusion to 0.35 m l . k g -1 .min -I exceeded the "filtration threshold" and arterial spillover occurred. They also demonstrated significant increases in pulmonary pressure and resistance, decreases in systemic pressure and cardiac output, and ST segment depression. These results are similar to those of Adornato et al. who showed that at 0.36 ml. kg -I 9min -l, a characteristic "gasp" was made, consisting of a small cough, a brief exhalation and then a period of forced inspiration that lasted several seconds, followed by apnoea for 10-30 seconds. 32 This "gasp," very similar to what the patients demonstrated, causes an acute decrease in central venous pressure, entraining more air and converting a sublethal embolism into a fatal one. Using Adornato's ("gasp") threshold infusion rate of 0.36 ml.kg -I .min -l, Patient 1 at 80 kg would have received 28.8 m l ' m i n -~, Patient 2 at 88 kg 31.68 ml. min- ~, Patient 3 at 64 kg 23.04 ml. min- l, Patient 4 at 82 kg 29.52 ml.min -1, and Patient 5 at 60 kg 21.6 ml.min -~. These figures are well below the 2.5-5 L. min- 1of air that could have been delivered by the drill, as estimated by the Bureau of Radiation and Medical Devices. Similarly, Artru and Colley, using dogs anaesthetized with nitrous oxide and isoflurane, determined 5 ml. kg -I of air injected over 30 seconds to be fatal. 35 Could the drill have delivered a lethal volume of air in the time of surgery to which the patients were submitted? Using the figure of 5 ml. kg -l, Patient ! would have received 400 ml, Patient 2 440 ml and Patient 3 320 ml.

119 Combining this value with the "gasp" threshold infusion rate, injection of the total volume of gas could have been delivered in 14 minutes; the arrests occurred 15, 30 and 50 minutes after the start of the procedure. The patients who collapsed all demonstrated similar signs: sudden collapse, loss of consciousness if awake, rapid development of cyanosis, absent pulse and quickly dilating pupils. In three patients, when monitoring was established by paramedics, EMD was seen. Those who died were difficult to resuscitate. Patient 2 underwent 16 minutes of paramedic resuscitation and Patient 3 an hour before a cardiac rhythm with output was established. Physicians were never able to restore a spontaneous rhythm with output in Patient 1. Similar problems in resuscitation have been reported after massive CO2 embolization. 36 Despite correct placement of a tracheal tube and ventilation with 100 per cent oxygen, cyanosis persisted in two of the patients. Patient 2 was still cyanosed on arrival at the hospital, 44 minutes after the arrest. Patient 1 had marked upper body cyanosis which persisted for at least 15 minutes after admission to hospital 11 minutes after arresting. A similar distribution of upper body cyanosis occurs in superior venacaval obstruction. Persistent cyanosis has been described after air embolism and may reflect a low cardiac output with consequent desaturation of venous haemoglobin. 3~ Arterial blood gas sampling showed marked hypoxia and hypercapnia in all three patients. Marked improvement was not seen until Patient 1 had 54 minutes, 2 had 86 minutes and 3 had 31 minutes of in-hospital resuscitation. Persistence of air in the pulmonary arterioles, increased shunting of pulmonary blood flow, and developing pulmonary oedema would hinder adequate gas exchange and prolong hypoxia and hypercarbia, despite apparently effective cardiac compression and lung ventilation. Elevated jugular venous pressures were seen in Patients 2 and 3 on arrival at hospital. These same patients showed electrocardiographic evidence of right bundle branch block and later, myocardial ischaemia. Electrocardiographic findings of ischaemia, particularly of the right heart, have been reported as a consequence of air embolism. 37 A chest x-ray taken after arrest showed pulmonary oedema in Patients 1, 2, and 3. Pulmonary oedema develops soon after air embolism 3s and is assumed to result from air, platelet and fibrin plugs in small vessels of the lungs, altering vascular resistance and hydrostatic balance. 38 Radiographic evidence may persist for 16-24 hours. 38'39 Finally, only one reference could be found of a death from air embolism during dental surgery. As Rickles and Joshi described, "a few minutes before death, pressurized air had been used extensively to clear the debris from the

120

canal of one of the patient's lower anterior teeth. During this procedure, the air tip was inserted into and held in the canal. Because of the emphysematous appearance of the face at autopsy, the pathologist tied off the great vessels and then, under water, opened into the right ventricle, from which a large quantity of air bubbled forth. ''4~ The authors went on to document the phenomenon in anaesthetized dogs and were able to produce air embolism by inserting a 21-gauge blunt cannula into the root canal and blowing air through it at 40-45 psi. The air was uniformly fatal if backflow from the cannula could be prevented by sealing it with self-curing acrylic resin, although an incomplete seal also allowed fatal results. Although the surgeon had not "sealed" the cannon drill into the mandible, he had produced the same effect. Firstly, the drill was designed to cut a precise hole in the mandible. Secondly, the presence of the mucoperiosteal flap could have acted as a "cover" over the drill to trap air in the mandible. Rickles and Joshi went on to state that an older animal did not succumb, although it had "an extremely emphysematous tongue and floor of the mouth," presumably because "the narrower apical foramen and the possibility of fewer vessels with thicker walls in the periapical region as compared with those of younger dogs prevented effective air embolization." This may explain why Patient 1 succumbed so quickly (and fatally), why Patients 2 and 3 could be resuscitated, why Patient 5 recovered from his cardiovascular collapse, and why Patient 4 suffered only massive subcutaneous emphysema. In conclusion, patients undergoing dental surgery are at risk of cardiovascular collapse. This may result from an exaggerated autonomic nervous system response to anxiety, from hypoxia, or from dysrhythmias induced by general or local anaesthetics (alone or mixed with epinephrine). Less often, as illustrated by these cases, the surgical procedure is the cause of the collapse. Anaesthetists should be aware of the complications of both the anaesthetic and the surgery and be prepared to recognise and treat them.

Acknowledgements The authors wish to thank the following physicians, Douglas B. Craig, Christopher J. Eagle, Henk Ter Keurs, and W. A. Tweed; Leigh C. Webber, LLB: members of the dental community of British Columbia, Messrs. M. Coyle, B. Douglas, B. Matthews, P. Ross, J. Waiters and Drs. R. N. Hicks and A. Swanson; and also the patients and family members of the patients, for their help with the investigation of these cases and preparation of the manuscript.

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