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CASE REPORT

VENOUS AIR-EMBOLISM DURING HYSTEROSCOPIC RESECTION OF UTERINE SEPTUM

Dr.SETHUNADH R, Dr. ARUNA RAJU, Dr. MANJUSHA S MENON

CARITAS HOSPITAL, THELLAKOM P.O, KOTTAYAM.

Address for correspondance:

Dr.Sethunadh R,Caritas Hospital

Thellakom,Kottayam, Kerala

[email protected]

INTRODUCTION

Venous air embolism (VAE) is an entity with the potential for severe morbidity and mortality.VAE is predominantly iatrogenic complication that occurs when atmospheric gas is introduced into systemic venous circulation. In past VAE was mostly associated with neuro surgical procedures conducted in sitting position.More recently VAE has been associated with central venous catherization, penetrating and blunt chest trauma, high pressure mechanical ventilation, thoracocentesis, haemodialysis, several other invasive vascular procedures and diagnostic studies-radio contrast injection for CT, use of carbon dioxide and nitrous oxide during medical procedures, and exposure to nitrogen during diving accidents.

Many cases of VAE are subclinical with no adverse outcome and thus go un-reported. Symptoms when present are nonspecific and a high index of clinical suspicion of possible VAE is required to prompt investigations and initiate appropriate therapy. Here we present a rare clinical scenario for VAE, during hysteroscopic resection of uterine septum under general anaesthesia in a33 year old female

CASE REPORT

33 year old female weighing 58kg was posted for hysteroscopic resection of uterine septum as a part of treatment of her infertility. She married 9 years back and she had five first trimester abortions.

She was hypertensive, taking atenolol 50mg once daily and blood pressure was controlled. She gives history of mild effort intolerance in the form of dyspnoea. She does not have any other medical or surgical illness. General and systemic examinations findings did not show any abnormalities.

She was premedicated with pantoprazole 40mg, metoclopramide 10mg and alprazolam 0.5mg at bedtime on pre-op day and two hours before surgery (6am on the day of surgery).She was kept nil by mouth since 10pm on pre-op day.

On entering the operation theatre an I.V. line secured with 18G cannula and fluid connected (RL).ECG, pulse-oxymeter, and automated NIBP are attached to the patient. Pre-op vital recordings were as follows

Pulse – 76/min

BP – 120/70mmHg

SpO2 – 98%

She was given glycopyrrolate 0.2mg, midazolam 1mg and fentanyl 100mcg immediately before induction. This is followed by lignocaine 60mg, propofol 100mg and succinylcholine 100mg I.V. Intubated with 7mm cuffed endotracheal tube. Air entry checked by 5 point auscultation and tube fixed. IPPV has given with oxygen (33%) nitrous oxide (66%) and isoflurane (1%).Vecuronium 4mg IV given.

After about 30mins of onset of surgery, patient’s SpO2 started falling along with disappearance of EtCO2 wave form. We rapidly checked the position of probe and side-stream tube connection and found to be correct. Meanwhile her blood pressure also started falling rapidly. The condition was clinically diagnosed as venous air embolism.

She was undergoing hysteroscopic septal resection during this incident Glycine was used to resect. Glycine was pumped into the uterus to distend it

with air pumping to the top of glycine level of bottle. Fluid finished un-noticed and air gushed in to the uterus

Suddenly surgeon stopped the procedure and took out resectoscope. We turned off nitrous oxide and isoflurane and IPPV given with 100% oxygen. Head down and left lateral position given to the patient. We cannulated the right IJV with 7F double lumen cannula using modified Seldinger technique, and through the cannula we could aspirate some amount of air (nearly 20ml).Both peripheral and carotid pulse were not palpable. Heart sounds were not audible but ECG shows activity (PEA).Heart rate also started falling. We gave chest compressions with patient turned supine and adrenaline 1mg through central line. Heart rate and BP increased and pulse became palpable SpO2 came above 90% and EtCO2 wave form appeared. We did a cardiology consultation and an echo was done and found bubbles in IVC, RA and RV. Echo repeated after resuscitation and showed mildly enlarged RA and RV, trivial TR, with good LV function.

Few minutes later she developed pulmonary oedema .We did ET tube suction and inj. Frusemide 40mg IV given. Pupils were dilated and we could not see a definite reaction to direct light. Patients started breathing spontaneously after about 1hour.We gave 600mg phenytoin and 16mg of dexamethazone IV. And we shifted the patient to ICU. Patient was ventilated in PS-PEEP mode (18-8cmH2O) with FiO2 of 0.8.Respiratory rate was 24/min and expiratory tidal volume was 400ml.We started dopamine infusion (5mcg/kg/min) and inserted a Ryle’s tube.

After about 2hours pupils started reacting and patient responded to pain.FiO2 gradually reduced to 0.4.ABG results were normal. We ventilated the patient in the same mode for about 36hours. Pulse,BP,CVP,SpO2,RBS,urine output, tidal volume, respiratory rate and pupillary reaction were monitored when the patient is on ventilator.ABG is done every 12 hours.

CXR, ECG, blood RE, PLC, electrolytes, PT results were normal during this period.CXR confirmed positions of ETT, RT and CVC.

After 36hours patient opened eyes spontaneously .Patient was connected to T-piece and extubated after two hours. After extubation she was managed with

Oxygen Nebulisation Chest Physiotherapy Steam Inhalation Deep Breathing Exercise and Incentive Spirometry Drugs

Following drugs were given in ICU

Inj. TAZACT 4.5gm IV TID Inj. DEXONA 8mg TID tapered Inj. PANTODAC 40mg OD Inj. PHENYTOIN 100mg TID oral Inj.DERIPHYLLINE 100mg TID oral Inj.TRAMADOL 50mg IV. SOS

We shifted the patient to ward after two days. She was having mild confusion and retrograde amnesia.

DISCUSSION

Two preconditions must exist for venous air embolism to occur: (1) a direct communication between a source of air and the vasculature and (2) a pressure gradient favouring the passage of air into the circulation.

The key factors determining the degree of morbidity and mortality in venous air emboli are related to the volume of gas entrainment, the rate of accumulation, and the patient’s position at the time of the event.

Generally, small amounts of air are broken up in the capillary bed and absorbed from the circulation without producing symptoms. Traditionally, it has been estimated that more than 5 mL/kg of air displaced into the intravenous space is required for significant injury (shock or cardiac arrest) to occur. However, complications have been reported with as little as 20 mL of air (the length of unprimed IV infusion tubing) that was injected intravenously. The injection of 2 or 3 mL of air into the cerebral circulation can be fatal. Furthermore, as little as 0.5 mL of air in the left anterior descending coronary artery has been shown to cause ventricular fibrillation. Basically, the

closer the vein of entrainment is to the right heart, the smaller the lethal volume is.

Rapid entry or large volumes of air entering the systemic venous circulation puts a substantial strain on the right ventricle, especially if this results in a significant rise in pulmonary artery (PA) pressures. This increase in PA pressure can lead to right ventricular outflow obstruction and further compromise pulmonary venous return to the left heart. The diminished pulmonary venous return will lead to decreased left ventricular preload with resultant decreased cardiac output and eventual systemic cardiovascular collapse

With venous air embolism (VAE), resultant tachyarrhythmias are frequent, but bradyarrhythmias can also occur.

The rapid ingress of large volumes of air (>0.30 mL/kg/min) into the venous circulatory system can overwhelm the air-filtering capacity of the pulmonary vessels, resulting in a myriad of cellular changes. The air embolism effects on the pulmonary vasculature can lead to serious inflammatory changes in the pulmonary vessels; these include direct endothelial damage and accumulation of platelets, fibrin, neutrophils, and lipid droplets.

Secondary injury as a result of the activation of complement and the release of mediators and free radicals can lead to capillary leakage and eventual non cardiogenic pulmonary oedema.

Alteration in the resistance of the lung vessels and ventilation-perfusion mismatching can lead to intra-pulmonary right-to-left shunting and increased alveolar dead space with subsequent arterial hypoxia and hypercapnea.

Arterial embolism as a complication of venous air embolism (VAE) can occur through direct passage of air into the arterial system via anomalous structures such as an atrial or ventricular septal defect, a patent foramen ovale, or pulmonary arterial-venous malformations. This can cause paradoxical embolization into the arterial tree. The risk for a paradoxical embolus seems to be increased during procedures performed in the sitting position.

Air embolism has also been described as a potential cause of the systemic inflammatory response syndrome (case report), triggered by the release of endothelium derived cytokines.

History

Most venous air emboli go unrecognized because their presentations are protean and mimic other cardiac, pulmonary, and neurologic dysfunctions. Because of the lack of specific signs and symptoms of venous air embolism (VAE), a high index of suspicion is necessary to establish the diagnosis and institute the appropriate treatment. The number of procedures that place patients at risk for VAE has increased, and these procedures occur across almost all clinical specialties. This must be considered to aid in the confirmation or ruling out of VAE. If venous air embolism is suspected, inquiry about the following key historical elements should be obtained:

Recent surgical procedures especially neurosurgical, otolaryngological, cardiovascular, or orthopaedic

Scuba diving trips and a history of decompression injuries or decompression sickness

Blunt or penetrating trauma to the head, face, neck, thorax, and/or abdomen

Invasive therapeutic and/or diagnostic procedures such as central venous catheterization; lumbar puncture; high-pressure infusion of medications, blood products, and/or IV contrast agents

Patients with HD access catheters or other indwelling central venous catheters

Patients on positive pressure ventilation Peripartum/postpartum orogenital sex (air may enter veins of the

myometrium) Ingestion of hydrogen peroxide (rare)

Physical

Clinical Presentation

Many cases of venous air embolism (VAE) are subclinical and do not result in untoward outcomes. However, severe cases are characterized by cardiovascular collapse and/or acute vascular insufficiency of several specific organs, including, but not limited to, the brain, spinal cord, heart, and skin. As mentioned earlier, the spectrum of effects is largely dependent on the rate and volume of entrained VAE.

Two additional contributing factors include whether or not the patient is spontaneously breathing (yielding negative thoracic pressure) or is under controlled positive pressure ventilation. These two factors facilitate the entry of air down a pressure gradient. The clinical presentation is also dependent on

the patient's body position at the time of the event. Generally, if the patient is in a sitting position, gas will travel retrograde via the internal jugular vein to the cerebral circulation, leading to neurologic symptoms secondary to increased intracranial pressure. In a recumbent position, gas proceeds into the right ventricle and pulmonary circulation, subsequently causing pulmonary hypertension and systemic hypotension. An arterial air embolism can also form if passage of air occurred through a right-to-left shunt, as in the case of a patent foramen ovale. The arterial air emboli can then lodge in the coronary or cerebral circulation, causing myocardial infarction or stroke.

Symptoms (awake patients)

Acute dyspnoea Continuous cough "Gasp" reflex (a classic gasp at times reported when a bolus of air enters

the pulmonary circulation and causes acute hypoxemia) Dizziness/light-headedness/vertigo

Nausea Sub-sternal chest pain Agitation/disorientation/sense of "impending doom"

Signs

Cardiovascular

Dysrhythmias (tachyarrhythmia/bradycardias) "Mill wheel" murmur - A temporary loud, machinery like, churning

sound due to blood mixing with air in the right ventricle, best heard over the precordium (a late sign)

JVD Hypotension Myocardial ischemia Nonspecific ST-segment and T-wave changes and/or evidence of right

heart strain Pulmonary artery hypertension Increased CVP Circulatory shock/cardiovascular collapse

Pulmonary

Adventitious sounds (rales, wheezing)

Tachypnoea Haemoptysis Cyanosis Decreased end-tidal carbon dioxide, arterial oxygen saturation, and

tension Hypercapnoea Increased pulmonary vascular resistance and airway pressures Pulmonary oedema Apnoea

Neurological

Acute altered mental status Seizures Transient/permanent focal deficits (weakness, paraesthesias, paralysis

of extremities) Loss of consciousness, collapse Coma (secondary to cerebral oedema)

Ophthalmologic

Fundoscopic examination may reveal air bubbles in the retinal vessels.

Skin

Crepitus over superficial vessels (rarely seen in setting of massive air embolus)

Livedo reticularis

The above hemodynamic, pulmonary, and neurologic complications primarily result from gas gaining entry into the systemic circulation, occluding the microcirculation and causing ischemic damage to these end organs. Animal studies have also suggested the presence of secondary tissue damage resulting from the release of inflammatory mediators and oxygen free radicals that occur in response to air embolism.

Causes

In order for venous air embolism (VAE) to occur, 2 physical preconditions for the entry of gas into the venous system must be met.

A direct communication between a source of air/gas and the vasculature (incising of noncollapsed veins) must exist.

A pressure gradient (sub atmospheric pressure in the vessels) favouring the passage of air into the circulation must be present.

Classically, venous air embolism has been recognized as occurring in the context of decompression illness in divers, aviators, and astronauts. Barotrauma and air emboli complicate an estimated 7 of every 100,000 dives.

However, the most common cause of VAE is iatrogenic.

Surgical procedures are the primary cause of venous air emboli. Neurosurgical procedures, especially those performed in the Fowler’s (sitting) position, and otolaryngological interventions are the two most common surgeries complicated by venous air emboli.

o The incidence of mild or clinically silent venous air embolism (VAE) during neurosurgical procedures has been estimated to range between 10% in cervical laminectomy surgeries where the patients are in the prone position, and 80% during posterior fossa surgeries (e.g., repair of cranial synostosis) where patients are placed in the Fowler’s position.

o Venous air emboli pose a risk anytime the surgical wound is elevated more than 5 cm above the right atrium. The presence of numerous, large, noncompressed, venous channels in the surgical field (especially during cervical procedures and craniotomies that breach the dural sinuses) also increase the risk of VAE.

Entrainment of air/gas facilitated by the patient's intraoperative position causing VAE may result from other surgical procedures. These include, craniofacial surgery, dental implant surgery, vascular procedures (e.g., endarterectomies), liver transplantation, orthopaedic procedures (e.g., hip replacement, spine surgery, arthroscopy), lateral decubitus thoracotomy, genitourinary surgeries in the Trendelenburg position, and surgeries involving tumours/malformations with high degree of vascularity or compromised vessels, as in the context of trauma.

Obstetric/gynaecological procedures (caesarean delivery) and laparoscopic surgeries each carry their own risk for venous air embolism. Although this risk is commonly not considered, they each have a reported associated incidence risk of VAE greater than 50%. The risk of

VAE during caesarean deliveries may be highest when the uterus is exteriorized. The risk of VAE in laparoscopic surgery may require an inadvertent opening of vascular channels through surgical manipulation rather than simply resulting from a complication of insufflation. Both of these surgical procedures have been associated with intraoperative mortality as direct sequele of air emboli. Despite this, the potential for venous air embolism is often ignored in laparoscopic surgery and caesarean delivery.

Venous air embolism may also result from the iatrogenic creation of a pressure gradient for air entry. Procedures causing such a pressure gradient include lumbar puncture (case report), peripheral intravenous lines, and central venous catheters.

Venous air embolism is a potentially life-threatening and under-recognized complication of central venous catheterization (CVC), including central lines, pulmonary catheters, haemodialysis catheters

and Hickman (long-term) catheters. As mentioned earlier, the frequency of VAE associated with CVC use ranges from 1 in 47 to 1 in 3000. The emboli may occur at any point during line insertion, maintenance, and/or removal. A pressure gradient of 5 cm H 2 O between air and venous blood across a 14-gauge needle allows the entrance of air into the venous system at a rate of 100 mL per second. Ingress of 300-500 mL of air at this rate can cause lethal effects. A number of factors increase the risk of catheter-related VAE, including the following:

o Fracture or detachment of catheter connections (accounts for 60-90%)

o Failure to occlude the needle hub and/or catheter during insertion or removal

o Dysfunction of self-sealing valves in plastic introducer sheathso Presence of a persistent catheter tract following the removal of a

central venous cathetero Deep inspiration during insertion or removal, which increases the

magnitude of negative pressureo Hypovolemia, which reduces central venous pressureo Upright positioning of the patient, which reduces central venous

pressure

Mechanical insufflation or infusion is another cause of venous air emboli.

o Several different procedures involve the use of insufflation, including arthroscopic procedures, CO 2 hysteroscopy, laparoscopy, urethral procedures, and orogenital sexual activity during pregnancy (by entering veins of the myometrium during pregnancy and/or after delivery).

o Inadvertent infusion of air can also occur during the injection of IV contrast agents for CT scans, angiography, and cardiac catheterization, as well as during cardiac ablation procedures. Little information exists on the incidence and the complication rate associated with iatrogenic air embolization caused by injections of contrast medium during CT examinations; however, this is a potentially serious complication, which could be catastrophic. Few case reports exist, and all agree that the actual number of such cases is probably higher than reported.

Positive pressure ventilation during mechanical ventilation places patients at risk for barotrauma and, subsequently, arterial and/or venous air emboli. Entry of gas into the circulation may result if violation of pulmonary vascular integrity occurs at the same time alveoli rupture from over distension of the airspaces. This complication can occur in the setting of various diagnoses; however, it is most frequently reported in patients with acute respiratory distress syndrome and in premature neonates with hyaline membrane disease. For these same reasons, SCUBA divers can also have VAE from alveolar distension.

The occurrence of venous air embolism (VAE) has also been described in the setting of blunt and penetrating chest and abdominal trauma as well as in neck and craniofacial injuries.

Differential DiagnosesAcute Coronary Syndrome Head Trauma

Anaemia, Acute Hypovolemia

Anaemia, Chronic Hypoxic brain injury

Angina Pectoris Intraparenchymal or subarachnoid haemorrhage

Aortic Stenosis Metabolic disorders (e.g., hypoglycaemia)

Atrial Fibrillation Myocardial Infarction

Atrial Flutter Pneumonia, Bacterial

Bronchospasm, acute Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum

Cardiogenic Shock Pneumothorax, Tension and Traumatic

Cerebral hypo perfusion Pulmonary thromboembolism

Chronic Obstructive Pulmonary Disease and Emphysema

Shock, Cardiogenic

Congestive Heart Failure and Pulmonary Oedema

Shock, Septic

Decompression Sickness Stroke, Hemorrhagic

Dissection, Aortic Stroke, Ischemic

Dysbarism

Electromechanical dissociation

Workup

Laboratory Studies

Laboratory tests are neither sensitive nor specific for the diagnosis of venous air embolism. The only indication for obtaining routine laboratory tests is to evaluate the associated end-organ injury resulting from air embolism.

Extravasation of fluid into inflamed tissue may result in laboratory findings consistent with intravascular depletion.

Arterial blood gas samples often show hypoxemia, hypercapnoea, and metabolic acidosis secondary to right-to-left pulmonary shunting.

Patients may develop a clinical picture similar to that of classic pulmonary embolism, with hypoxia, decreased PCO 2 levels, and respiratory alkalosis.

Imaging Studies

Trans oesophageal echocardiography (TEE) has the highest sensitivity for detecting the presence of air in the right ventricular outflow tract or major pulmonary veins. It can detect as little as 0.02 mL/kg of air administered by bolus injection. It also has the added advantage of identifying paradoxical air embolism (PAE), and Doppler allows audible detection of venous air embolism (VAE). Echocardiography, both TEE and trans thoracic echocardiography (TTE) not only allow for the diagnosis of VAE but also aid in the diagnosis of cardiac anomalies, assessment of volume status, pulmonary hypertension, and cardiac contractility, thereby allowing exclusion of other causes of hypotension, dyspnoea, and aiding in further patient management. The use of bedside TTE has become more common in emergency medicine. Its use in a case of VAE described by Maddukuri et al aided in the diagnosis and prompt initiation of appropriate therapy.

Precordial Doppler ultrasonography is the most sensitive non-invasive method for detecting venous air emboli. This modality is capable of detecting as little as 0.12 mL of embolized air (0.05 mL/kg).

Trans cranial Doppler ultrasonography is another imaging modality commonly used to detect cerebral micro emboli.

Chest radiography may be normal or may show gas in the pulmonary arterial system, pulmonary arterial dilatation, focal oligemia (Westermark sign), and/or pulmonary oedema.

CT scans can detect air emboli in the central venous system (especially the axillary and subclavian veins), right ventricle, and/or pulmonary artery. Small (<1 mL) air defects, usually asymptomatic, occur during 10-25% of contrast-enhanced CT scans; thus, the specificity of this modality is best with large filling defects. CT scans of the head may show intra cerebral air, cerebral oedema, or infarction. Chest CT in lung trauma may show underlying conditions such as pneumothorax, hemothorax, or emphysematous blebs that may have led to air embolism but is not helpful for initial diagnosis.

MRI of the brain may show increased water concentration in affected tissues, but this finding alone may not be reliable for the detection of gas emboli.

Other Tests

Electrocardiographic (ECG) – Low sensitivity for venous air embolism (VAE) detection. The findings closely resemble those seen with venous thromboembolism and include tachycardia, right ventricular strain pattern, and ST depression. Transient myocardial ischemia may also

occur (severe bradycardia, ST elevation in inferior leads and ST depression in L1 and avL, observed 3 minutes post CVC removal (case report).

End-tidal carbon dioxide (ETCO2) – VAE leads to V/Q mismatching and increases in physiologic dead space. This produces a fall in end-tidal CO2 (normal value is <5). A change in 2 mm Hg ETCO2 can be an indicator of VAE. However, this finding is nonspecific and may also occur with other disease states, such as pulmonary embolism (PE), massive blood loss, hypotension, circulatory arrest, upper airway obstruction, mouth breathing, and/or disconnection from monitor. The detector also has a slow response time.

End-tidal nitrogen (ETN2) – Most sensitive gas-sensing VAE detection modality; measures increases in ETN2 as low as 0.04%. Response time is much faster than ETCO2 (30-90 s earlier). However, it does not detect subclinical VAE or decreases with hypotension and may falsely indicate resolution of VAE too prematurely.

Pulse oximetry – Changes in oxygen saturation are late findings with VAE. Measurement is often skewed secondary to exposure to high fraction inspired oxygen. Like carbon dioxide measuring, it is on the lower end of sensitive measurements.

Pulmonary artery catheter – Can detect increases in pulmonary artery pressures, which may be secondary to mechanical obstruction/vasoconstriction from the hypoxemia induced by the VAE. However, it is a relatively insensitive/nonspecific monitor of air entrainment (0.25 mL/kg). The lumen catheter is also too small for air to be removed, thereby limiting its function.

Central venous catheter – If in place, aspiration of air may help make the diagnosis. It is also helpful in monitoring central venous pressures, which may be increased in VAE.

Procedures

Any procedure posing a risk for venous air embolism (VAE), if in progress, should be aborted immediately once VAE is suspected.

During central venous catheterization (CVC) insertion/removal, one attempt at aspirating air back from line may be useful. Prior to aspiration, the tip of the central venous catheter should be optimally placed 2 cm below the junction of the SVC and the right atrium; however, it may need to be advanced to optimize results. If not already in place, the placement of a CVC (multi orifice) or PA catheter to attempt aspiration of air has been recommended by several authors. When

appropriately placed, it may be possible to aspirate approximately 50% of the entrained air with a right atrial catheter. Catheter removal should be performed with the patient supine or in a Trendelenburg position while holding his/her breathe at the end of inspiration or during a Valsalva maneuver.

In the event of circulatory collapse, CPR should be initiated in order to maintain cardiac output. CPR may also serve to break large air bubbles into smaller ones and force air out of the right ventricle into the pulmonary vessels, thus improving cardiac output.

If an arrest is refractory to CPR, an immediate thoracotomy in the ED may be indicated. An emergency thoracotomy with clamping of the hilum of the injured lung is currently recommended for SAE-associated with unilateral lung injury. This prevents continued passage of air into the coronary, cerebral, and other systemic arteries.

Other measures include cross-clamping the aorta, cardiac massage, and aspirating air from the left ventricle, aortic roots, and pulmonary veins.

Treatment

Pre hospital Care

If venous air embolism (VAE) is known about prior to ED presentation, these patients should be transported in the left lateral decubitus position.

Emergency Department Care

Management of venous air embolism (VAE), once is suspected, includes identification of the source of air, prevention of further air entry (by clamping or disconnecting the circuit), a reduction in the volume of air entrained, and hemodynamic support.

Administer 100% O 2 and perform endotracheal intubation for severe respiratory distress or refractory hypoxemia or in a somnolent or comatose patient in order to maintain adequate oxygenation and ventilation. Institution of high flow (100%) O 2 will help reduce the bubble's nitrogen content and therefore size.

Immediately place the patient in the left lateral decubitus (Durant maneuver) and Trendelenburg position. This helps to prevent air from travelling through the right side of the heart into the pulmonary arteries,

leading to right ventricular outflow obstruction (air lock). If CPR is required, place the patient in a supine and head-down position.

Direct removal of air from the venous circulation by aspiration from a central venous catheter in the right atrium may be attempted. However, no current data support emergent catheter placement for air aspiration during an acute setting of VAE-induced hemodynamic instability.

If necessary, initiate CPR. Other than maintaining cardiac output, CPR may also serve to break large air bubbles into smaller ones and force air out of the right ventricle into the pulmonary vessels, thus improving CO. Even without the need for CPR, this rationale holds for closed-chest massage. Animal studies have shown that the benefit of cardiac massage equals that of left lateral recumbency, as well as intra cardiac aspiration of air.

Consider transfer to a hyperbaric oxygen therapy (HBOT) facility. Indications for HBOT include neurological manifestations and cardiovascular instability. Potential benefits include compression of existing bubbles, establishing a high diffusion gradient to speed resolution of existing bubbles, improved oxygenation of ischemic tissues, and lowered intracranial pressure. Immediate HBOT, once venous air embolism (VAE) is diagnosed, is recommended; however, prognosis may still be good if therapy is initiated beyond 6 hours of event. Prompt transfer to an HBOT centre has been reported to decrease the mortality rate in patients with cerebral air embolism. If transfer is necessary, ground transportation is preferred. If air transportation cannot be avoided, the lowest altitude should be sought.

Supportive therapy should include fluid resuscitation (to increase intravascular volume, increase venous pressure and venous return). Also some evidence exists that gas emboli may cause a relative haemoconcentration, which increases viscosity and impairs the already compromised circulation. Hypovolemia is less tolerated than relative anaemia. In animal studies, moderate haemodilution to a hematocrit of 30% reduces neurologic damage. Crystalloids may cause cerebral oedema; therefore, colloids are preferred for hemodilution.

The administration of vasopressors and mechanical ventilation are two other supportive measures that may necessary. In a case report of a patient undergoing a craniotomy who showed cardiopulmonary findings suggestive of acute venous air embolism, inotropic treatment with ephedrine seemed to rapidly reverse the cardiopulmonary abnormalities. Early inotropic support of the right ventricle has been recommended if venous air embolism is suspected.

In animal studies, the use of per fluorocarbons (FP-43) has been shown to enhance the reabsorption of bubbles and the solubility of gases, thereby decreasing both the neurologic and cardiovascular complications of systemic and coronary venous air embolism. These benefits, however, have not been validated in humans.

Follow-up

Further Inpatient Care

Admit patients to the intensive care unit (ICU), as they may develop cardiopulmonary distress/failure following venous air embolism (VAE).

Transfer

Consider transfer to a hyperbaric medicine centre for symptomatic venous air embolism.

Deterrence/Prevention

The optimal management of venous air embolism (VAE) is prevention.

Minimizing the pressure gradient between the site of potential entry and the right atrium is essential in prevention of VAE.

Measures to reduce the risk of air embolism during mechanical ventilation and central line insertion/removal/manipulation should be taken. With regard to these two procedures, the following interventions should be implemented:

o Prevent barotraumas by minimizing airway pressures during mechanical ventilation.

o Avoid PEEP as it impairs hemodynamic performance, does not protect against air embolism, and probably increases risk of paradoxical emboli.

o Avoid and treat hypovolemia prior to catheter placement.o Occlude the needle hub during catheter insertion/removal.

o Maintain all connections to the central line closed/locked when not in used (use Luer-lock syringes for blood draws from catheters).

o During catheter insertion/removal, place the patient in the supine position with head lowered (insertion site should be 5 cm below right atrium). If the patient is awake he or she may assist by holding his or her breath or by doing a Valsalva maneuver, both of which can increase the central venous pressure

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