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Home , Air embolism, Embolism

Air - A Case Series and Review

S. SVIRI*†, W. P. D. WOODS*, P. V. VAN HEERDEN*‡ *Department of Intensive Care, Sir Charles Gairdner Hospital, Nedlands, WESTERN AUSTRALIA †Medical Intensive Care Unit, Hadassah Hospital, Jerusalem, ISRAEL ‡School of Medicine and Pharmacology, University of Western Australia, Crawley, WESTERN AUSTRALIA

ABSTRACT Venous or arterial may be a life threatening event. The condition is seen in many fields of medicine, including intensive care. We present a series of three cases of air embolism encountered in the intensive care unit, which demonstrate different pathophysiologies for air embolism in critically ill patients. We also review the literature with respect to aetiology, incidence, pathophysiology, diagnosis and treatment options for venous and arterial embolism. (Critical Care and 2004; 6: 271-276)

Key words: Air embolism, cardiopulmonary resuscitation, aetiology, management

Air embolism can be a serious and even fatal event source of his sepsis. He was admitted, and intravenous in the intensive care unit (ICU). The ICU is a setting amoxicillin and flucloxacillin were commenced. Subs- where most patients have central venous or equently, the patient became tachypnoeic and developed undergo procedures which may put them at risk.1 septic shock with a of 80/60 mmHg, Patients may also present with post operative air of 39ºC and arterial saturation 1,2 embolism as a . A high level of vigilance (SaO2) of 90% ( oxygen at 10 L/min through a should be maintained, to allow for prompt diagnosis and non-rebreathing mask). The antibiotics were changed to rapid treatment of this condition. ticarcillin and gentamicin. On further questioning, the We present three cases of air embolism in the ICU patient claimed he had undergone rectal trauma with a and review the literature regarding aetiology, incidence, broom handle, prior to his first presentation. As his pathophysiology and treatment of air embolism. condition continued to deteriorate he was transferred to our hospital. CASE REPORTS In the emergency department he was agitated with a Patient 1. A 45-year-old man with a past history of 116/80 mmHg, rate 120 beats per intravenous drug abuse, heavy ethanol intake and min, temperature 37.2ºC, tachypnoeic and hypoxic with positive serology for Hepatitis C virus, was transferred bibasal crepitations heard on auscultation. There was no to our ICU from another hospital. His presenting cardiac murmur. His abdomen was soft, without organ- problems were sepsis and cardiorespiratory failure. omegally and altered blood was found on rectal examin- He presented initially to the peripheral hospital ation. Intravenous ‘track’ marks were noted between his complaining of transient right sided weakness. On toes. Neurological examination was unremarkable. A examination a right molar tooth abscess was found and a chest X-ray demonstrated bilateral alveolar infiltrates. computed tomography (CT) scan of his cranium showed Due to progressive respiratory distress the patient an old left frontal infarct. The patient underwent molar was intubated and mechanically ventilated. A cranial CT extraction in the emergency department as he refused was performed which showed an acute left cerebellar admission. infarct and an old left frontal infarct. An abdominal CT The patient returned to the peripheral hospital three showed in the middle hepatic , an absent left days later with a high fever, , rigors and kidney, with compensatory hypertrophy of the right . Initial examination failed to reveal a kidney, and a normal peri-rectal area.

Correspondence to: Dr. P. van Heerden, Department of Intensive Care, Sir Charles Gairdner Hospital, Nedlands, Western Australia 6009 (e-mail: [email protected])

271 S. SVIRI, ET AL Critical Care and Resuscitation 2004; 6: 271-276

The patient was transferred to the ICU, where he was sedated and ventilated with an inspired oxygen concen- tration of 70%. He required intravenous adrenaline to maintain his blood pressure. He remained oliguric with rising plasma urea and creatinine levels. A bedside sigmoidoscopy was performed to exclude a rectal or sigmoid perforation which revealed blood in the lower rectum, although the mucosa, up to 15 cm, appeared to be normal. Shortly after the sigmoidoscopy the patient became cyanosed, bradycardic and subseque- ntly became asystolic. Cardiopulmonary resuscitation was commenced and the patient was given adrenaline, atropine, isoprenaline, intravenous colloids and placed in the head down, right side up position, as an air embolism from the sigmoidoscopy was suspected. Aspiration of blood from the central venous did not reveal air. External pacing was initiated but no pulse could be felt. He subsequently died. A chest x-ray was taken during the resuscitation which showed a large amount of air within the cardiac silhouette (figure 1). A post mortem chest CT demonstr- Figure 2. Chest computerised tomography performed post-mortem ated a large amount of air in the right ventricular showing a large amount of air in the right ventricular outflow tract. outflow tract (figure 2) and a post mortem abdominal CT showed extensive air within the hepatic . Patient 2. An 85-year-old man underwent urgent femoral-popliteal bypass surgery at another hospital to manage a left gangrenous foot. His past history included severe peripheral vascular , chronic ischaemic cardiac disease with congestive and type 2 mellitus. Post operatively he was transferred to the ICU, where he was found to be hypotensive. As he remained hypotensive in spite of crystalloid infusions, Haemaccell® (Hoechst Marion Roussel, Lane Cove, NSW) was prescribed and a needle was inserted into the top of the bottle to increase the administration rate. As the rate of fluid flow was still deemed to be inadequate, a pressure bag was placed on the bottle and the needle hole sealed with tape. Several minutes later, the patient became profoundly shocked and bradycardic. An air embolism was suspected and CPR was initiated.

As there was no central venous access, air could not be Figure 1. Antero-posterior chest X-ray showing intracardiac air. aspirated. Resuscitation attempts failed and the patient died. A post-mortem chest X-ray revealed a large The post mortem examination revealed an intestinal amount of intra-cardiac air (figure 3) and at post mortem perforation 15 cm from the ano-rectal margin extending examination, air was found in the cerebral vessels as 5 cm along the circumference of the bowel wall. The well as the cardiac chambers. perforation was adjacent to iliac veins and probably provided a passage for air to travel into the inferior vena Patient 3. A 26-year-old female was admitted to cava at the time of the sigmoidoscopy. Within the aorta hospital for biopsy of a recurrent pineal lesion and and ventricles frothy blood was noted. The were underwent posterior fossa craniotomy in the sitting consolidated, consistent with acute respiratory distress position. During the procedure the anaesthetist noted syndrome (ARDS). A 15 mm right upper lobe abscess three episodes of profound and decreased was noted. A recent haemorrhagic in the left end tidal carbon dioxide . For each cerebellum and multiple small cerebral haemorrhages episode the operative field was flooded with were seen and small air bubbles noted within the , the patient lowered to a supine position and air cerebral vessels. was aspirated from a .

272 Critical Care and Resuscitation 2004; 6: 271-276 S. SVIRI, ET AL

when air is forced under pressure directly or indirectly into the bloodstream1,2 (e.g. cases 1 and 2).

Aetiology The causes of air embolism include entry of air through intravascular catheters such as peripheral and central venous canulae, pulmonary catheters, haemodialysis catheters, pressurised infusion systems and long term central catheters such as Hickman catheters.1,4 Entry of air during surgery may be common, especially during neurosurgery, laparoscopic surgery and cardiothoracic surgery.1,3,5,6 The risk of air embol- ism is particularly high in neurosurgical procedures performed in patients in the sitting position. The

Figure 3 Lateral chest X-ray demonstrating intracardiac air. incidence of air embolism is 10% for cervical laminect- 5 omies and up to 80% in posterior fossa surgery. This is Post operatively the patient was transferred to the due to the pressure gradient between ambient air and the ICU, where she was hypotensive, tachycardic, confused exposed venous circulation in the head during the sitting and hypoxic. A chest x-ray was consistent with position where the venous pressure is negative with pulmonary oedema and an ECG showed diffuse ST and respect to the heart. In the ICU, special care must be T wave changes. She was reintubated, ventilated with taken to avoid air embolism via intravenous and arterial 4,7 100% oxygen, positioned in the left lateral decubitus catheters, catheters and intra-aortic position and intravenous adrenaline was infused. A balloon catheters. During positive pressure ventilation, cranial CT performed the following morning showed has also been described as causing air 1 extensive bilateral cortical and subcortical infarcts with embolism. Insufflation of air into a body cavity during diffuse cerebral oedema. Her best neurological response endoscopy can also cause air to enter the circulation a week later consisted of spontaneous eye opening but (e.g. case 1). no response to voice or pain. A transthoracic echocard- Radiological procedures such as and iogram demonstrated normal ventricular function and no during the of air as a contrast agent have also 1 evidence of an atrioseptal or ventriculoseptal defect. been implicated in venous and arterial air embolism, as 8 One month later good cognitive function and have cardiac catheterisations and cardiac ablation 9 memory returned. An MRI of the before discharge procedures. Other high risk procedures include radical demonstrated a small residual pineal tumour and an neck surgery, obstetric and gynecological procedures 10 extensive anterior and posterior watershed ischaemic including Cesarean sections and laparoscopic surgery, in keeping with global cerebral hypoperfusion. (for example endarterectomies) and Four months later she was wheelchair bound but was orthopaedic surgery (such as hip replacement, spine 1,5 communicating adequately with her family. surgery and arthroscopy). Cases of air embolism have also been described in DISCUSSION and REVIEW trauma such as blunt and penetrating chest trauma, Air embolism, or the entry of air into the circulation, , neck and craniofacial and 1 is mostly an iatrogenic problem but may also occur with injury . Air embolism has also been trauma.1,2 Air commonly enters the venous system but described as a result of orogenital sexual activity during may also enter the arterial system. The disorder may . include other than air including carbon dioxide and nitrous oxide, which are used in medical Pathophysiology procedures, and nitrogen, usually found in diving In 1947 Durant studied air embolism in dogs and accidents.1,3 Air embolism may have disastrous cardiac, reported that the most important factors determining pulmonary or neurological effects and is associated with mortality were the amount of air entering the blood- a high morbidity and mortality.1 stream, the speed with which it enters and the body 11 The entry of air into the blood stream requires a position at the time of embolism. Rapid entry of air pressure gradient favouring the passage of gas into the into the circulation may cause severe haemodynamic .2 This occurs when venous pressure is instability. A fatal dose is considered to be 300 - 500 negative relative to (e.g. case 3) or mL of air at a rate of 100 mL/sec; a rate which is

273 S. SVIRI, ET AL Critical Care and Resuscitation 2004; 6: 271-276 possible with a 14 gauge needle and a pressure gradient Central venous catheters 2,5 of only 5 cm H2O between air and venous blood. In The frequency of venous air embolism reported with the critically ill, unstable patient, smaller volumes of air central catheters has ranged from 1 in 47 to 1 in 3000 may also be fatal. catheters.2 The mortality associated with this event When a large bolus of air rapidly enters into the reaches 30%. As air may enter whenever venous venous system, it causes an air lock in the right pressure decreases below ambient air pressure, the risk and causing right ventricular outflow obstruct- is increased during deep inspiration, hypovolaemia, ion and death. With slow entry of air into the right strained respirations and when the patient is in the ventricle, obstruction occurs at the level of the pulmon- upright position. Most cases occur during catheter ary vasculature, causing vasoconstriction and pulmonary manipulation, disconnection, hub fracture or removal, . Small amounts of air may be tolerated, as and not only during central venous catheter insert- air is absorbed from the circulation, but large amounts ion.15,16 Catheter removal should be performed with the of air may result in right ventricular strain, decreased patient supine or in the Trendelenburg position, while cardiac output, shock and death.1,5 holding his or her breath at the end of inspiration or during a .17 In mechanically ventil- ated patients the catheter should be removed at end Cardiac manifestations of air embolism include chest inspiration, when the pressure in the chest is more than pain and light-headedness.2 The typical “mill-wheel” atmospheric pressure. Direct pressure should be applied murmur that has a splashing sound may be heard with a on the catheter site for several minutes after bleeding precordial or oesophageal stethoscope, but is generally a has stopped18 and an occlusive dressing should be late sign. Electrocardiographic changes include non- placed over the exit site.19 specific ST and T wave changes and evidence of right ventricular strain.2 Diagnosis The patient may also develop bradyarrhythmias or The diagnosis of venous air embolism relies on a tachyarrhythmias. Pulmonary artery are high index of suspicion in high risk cases (e.g. decreased in a “bolus” air and increased in neurosurgical procedures in the sitting position, etc). “slow” air embolism.2 Central venous pressures are Sudden hypotension, and bradycardia, increased due to right ventricular failure and the patient aspiration of air bubbles through a central catheter and may become haemodynamically compromised. In severe characteristic cardiac sounds all aid in the diagnosis. cases, asystole or pulseless electrical activity may occur The precordial stethoscope may help in detecting a leading to death. “mill-wheel” murmur, but this often difficult to hear and Respiratory manifestations include dyspnoea or may develop late in the patient’s condition.2,5 End-tidal tachypnoea and the classic “gasp” reflex due to acute carbon dioxide monitoring is convenient and practical hypoxaemia.2,5 Neutrophils release cytokines in the and with air embolism it decreases as a result of increa- causing damage and increased permeability that is sed caused by an obstruction of pulmonary similar to ARDS.2 Patients may develop a deterioration . Precordial Doppler ultrasound is a sensitive and in lung function, with reduced compliance, increased noninvasive and may detect small amounts of air by dead space and shunting leading to hypoxaemia and converting changes in blood density into sound.2,5 hypercarbia.12 has also been used to detect The term “” is used to describe cerebral microemboli during endovascular procedures.8 situations in which gas crosses into the left atrium The most sensitive monitoring device is the trans- through a patent or , oesophageal echocardiograph which may detect as little thus causing air embolism within the systemic as 0.02 mL/kg of air and air bubbles as small as 5 - 10 circulation.13 This may cause cardiac and neurological microns. Transoesophageal echogardiography (TOE) manifestations, although neurological deficits may may also identify the cardiac location of air bubbles and develop as a result of prolonged hypoxaemia and shock may demonstrate the passage of air into the left as well as direct air embolism. There have been several atrium.2,5,14,20 cases of systemic air embolism due to venous embolism where a cardiac defect could not be found. It is Treatment presumed that air can also enter the systemic circulation The source of air must be identified and further through physiological pulmonary right to left shunts or vascular entry of air stopped. Operative fields should be due to passage of air into the left atrium via the flushed with saline, central lines secured or removed pulmonary veins.14 etc.5 Air may be evacuated from the right atrium or

274 Critical Care and Resuscitation 2004; 6: 271-276 S. SVIRI, ET AL ventricle via a central venous catheter or a pulmonary and increases oxygen in plasma thereby artery catheter with up to 50% of air aspirated depend- improving oxygen tissue delivery.1,22 In a recent review,1 ing on catheter placement and patient positioning.2,5 It hyperbaric was recommended in all has been shown that optimal placement of the catheter patients with arterial air embolism. Although there have tip for aspiration of air is 2 cm below the junction of the been many promising results, even with delayed superior vena cava and right atrium.5 treatment, the efficacy of this treatment has yet to be Supportive therapy for the patient with air embolism proven, especially when taking into consideration the includes intravascular volume to increase venous pressu- logistic difficulties involved and the cardiovascular res and venous return, intravenous catecholamines and instability of these patients.15,23 mechanical ventilation1,5,21. Cardiopulmonary resuscitat- Intraoperative retrograde cerebral has been ion may be used as a means of maintaining cardiac used with a good neurological outcome for a proven output but may also serve to break large air bubbles into arterial air embolism in a 5-year-old girl undergoing smaller ones and air out of the right ventricle into repair of an atrial-septal defect together with post- the pulmonary vessels, thus improving cardiac output.2 operative barbiturate induced anaesthesia and hyper- Oxygenation is important, not only to increase haemo- baric oxygen therapy.22 Other treatments, such as globin saturation and improve peripheral tissue intravenous lignocaine, corticosteroids and heparin1 oxygenation, but also to reduce size, as 100% have been suggested for the management of arterial air oxygen will reduce the nitrogen content and size of the embolism but none of these have been shown to be air bubble.1,5 effective. Patient positioning has been shown to be important. 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