**Fat Embolism in Orthopedic Surgery**

Ismet Gavrankapetanović, Adnan Papović, Mehmed Jamakosmanović, Elvir Baždar and Lejla Tafro

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/67710

#### **Abstract**

[27] Northup PG, McMahon MM, Ruhl AP, Altschuler SE, Volk‐Bednarz A, Caldwell SH, et al. Coagulopathy does not fully protect hospitalized cirrhosis patients from peripheral

[28] Dabbagh O, Oza A, Prakash S, Sunna R, Saettele TM. Coagulopathy does not protect against venous thromboembolism in hospitalized patients with chronic liver disease.

[29] Smith CB, Hurdle AC, Kemp LO, Sands C, Twilla JD. Evaluation of venous thrombo‐ embolism prophylaxis in patients with chronic liver disease. J Hosp Med. 2013; **8**(10):

[30] Zhang X, Qi X, De Stefano V, Hou F, Ning Z, Zhao J, et al. Epidemiology, risk factors, and in‐hospital mortality of venous thromboembolism in liver cirrhosis: a single‐center

[31] Lesmana CR, Inggriani S, Cahyadinata L, Lesmana LA. Deep vein thrombosis in patients with advanced liver cirrhosis: a rare condition? Hepatol Int. 2010; **4**(1): 433‐8.

[32] Barclay SM, Jeffres MN, Nguyen K, Nguyen T. Evaluation of pharmacologic prophylaxis for venous thromboembolism in patients with chronic liver disease. Pharmacotherapy.

[33] Walsh KA, Lewis DA, Clifford TM, Hundley JC, Gokun Y, Angulo P, et al. Risk factors for venous thromboembolism in patients with chronic liver disease. Ann Pharmacother.

[34] Sogaard KK, Horvath‐Puho E, Montomoli J, Vilstrup H, Sorensen HT. Cirrhosis is asso‐ ciated with an increased 30‐day mortality after venous thromboembolism. Clin Transl

[35] Montomoli J, Erichsen R, Sogaard KK, Kormendine Farkas D, Bloch Munster AM, Sorensen HT. Venous thromboembolism and subsequent risk of cancer in patients with liver disease: a population‐based cohort study. BMJ Open Gastroenterol. 2015; **2**(1):

retrospective observational study. Med Sci Monit. 2016; **22**: 969‐76.

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94 Embolic Diseases - Unusual Therapies and Challenges

569‐73.

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Every long bone fracture in orthopedic surgery represents a possible scenario for development of embolism complication, especially the fat embolism. There is no scientific explanation why fat embolism occurs and what are the hypotheses for development of fat embolism or the proper way of prevention, but just speculations and possible theories in the evolution of the clinical picture of fat embolism syndrome. Throughout this chapter, the authors will explain the possible theories of development of fat embolism, risk factors, pathology, and pathophysiology during progress of the clinical picture and signs of the fat embolism syndrome and therapy.

**Keywords:** fat embolism, orthopedic surgery, complications, fractures

#### **1. Introduction**

Every long bone fracture in orthopedic surgery represents a possible scenario for development of embolism complication, especially the fat embolism.

#### **2. History**

In 1861, fat embolism was first described by Zenker after a railroad accident and a worker who sustained crush syndrome injuries [1]. At the time when it was first described, it was believed that fat from the bone marrow, after a long bone fracture, embolized in the lungs causing pulmonary deficiency. On the other hand, Fenger and Salisbury believed that fat embolized from

© 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

fractures to the brain causing death [2]. Von Bergmann first clinically diagnosed fat embolism in a patient with a fractured femur in 1873 [3]. Fat embolism was thoroughly monitored and described during World Wars I and II. It was noted by Wong and his colleagues that patients with long bone fractures had a couple of desaturation episodes during the day with prolonged period of total desaturation [4].

#### **3. Pathophysiology of fat embolism**

The pathophysiologic mechanism of fat embolism is comprised of two theories—mechanical obstruction and biochemical injury. After a long bone fracture, fat emboli together with erythrocytes and thrombocytes can occlude pulmonary or brain blood vessels. The release of free fatty acids from fat causes local toxic effect on the endothelium, while the activation of platelets and granulocytes causes vascular incident.

Mechanical obstruction of the pulmonary blood vessels occurs because of the size of the embolized particles. In a dog model, Teng and colleagues found 80% of fat droplets to be between 20 and 40 μm, while vessels in the lungs that are smaller than 20 μm become obstructed [5]. Fat globules of 10–40 μm have been found after human trauma [6].

The biochemical theory suggests that mediators from the fracture site alter lipid solubility, causing coalescence, because normal chylomicrons are smaller than 1 μm. Many of the emboli have a histological composition consisting of a fatty center with platelets and fibrin adhered [7]. Large amounts of thromboplastin are liberated with the release of the bone marrow, leading to the activation of the coagulation cascade.

Peltier hypothesized that elevated serum lipase levels present after the embolization of neutral fat hydrolyzes this neutral fat to free fatty acids and causes local endothelial damage in the lungs and other tissues, resulting in FES [8]. This chemical phase might in part explain the latency period seen between the arrival of embolic fat and more severe lung dysfunction. Elevated serum lipase levels have been reported in association with clinically fatal FES [9, 10].

Mudd and colleagues did not find any myeloid tissue in any of the lungs at autopsy in patients with FES and suggested that the soft tissue injury, rather than fractures, was the primary cause of FES [11].

#### **4. Incidence**

The incidence of fat embolism is still not completely known. From the studies done on this topic so far, it happens in younger patients more often with lower limb fractures. Its incidence rises with the number of fractured long bones and severity of suffered injuries. Chan and associates found an incidence of 8.75% of overt FES in all fracture patients, with a mortality rate of 2.5% [12]. The incidence rose to 35% in patients with multiple fractures. Other investigators reported the incidence of FES between 0.9 and 3.5% in patients with long bone fractures [13–15].

#### **5. Clinical presentation**

fractures to the brain causing death [2]. Von Bergmann first clinically diagnosed fat embolism in a patient with a fractured femur in 1873 [3]. Fat embolism was thoroughly monitored and described during World Wars I and II. It was noted by Wong and his colleagues that patients with long bone fractures had a couple of desaturation episodes during the day with pro-

The pathophysiologic mechanism of fat embolism is comprised of two theories—mechanical obstruction and biochemical injury. After a long bone fracture, fat emboli together with erythrocytes and thrombocytes can occlude pulmonary or brain blood vessels. The release of free fatty acids from fat causes local toxic effect on the endothelium, while the activation of platelets

Mechanical obstruction of the pulmonary blood vessels occurs because of the size of the embolized particles. In a dog model, Teng and colleagues found 80% of fat droplets to be between 20 and 40 μm, while vessels in the lungs that are smaller than 20 μm become obstructed [5].

The biochemical theory suggests that mediators from the fracture site alter lipid solubility, causing coalescence, because normal chylomicrons are smaller than 1 μm. Many of the emboli have a histological composition consisting of a fatty center with platelets and fibrin adhered [7]. Large amounts of thromboplastin are liberated with the release of the bone marrow, leading to

Peltier hypothesized that elevated serum lipase levels present after the embolization of neutral fat hydrolyzes this neutral fat to free fatty acids and causes local endothelial damage in the lungs and other tissues, resulting in FES [8]. This chemical phase might in part explain the latency period seen between the arrival of embolic fat and more severe lung dysfunction. Elevated serum lipase levels have been reported in association with clinically fatal FES [9, 10]. Mudd and colleagues did not find any myeloid tissue in any of the lungs at autopsy in patients with FES and suggested that the soft tissue injury, rather than fractures, was the primary

The incidence of fat embolism is still not completely known. From the studies done on this topic so far, it happens in younger patients more often with lower limb fractures. Its incidence rises with the number of fractured long bones and severity of suffered injuries. Chan and associates found an incidence of 8.75% of overt FES in all fracture patients, with a mortality rate of 2.5% [12]. The incidence rose to 35% in patients with multiple fractures. Other investigators reported the incidence of FES between 0.9 and 3.5% in patients with long bone

Fat globules of 10–40 μm have been found after human trauma [6].

longed period of total desaturation [4].

96 Embolic Diseases - Unusual Therapies and Challenges

**3. Pathophysiology of fat embolism**

and granulocytes causes vascular incident.

the activation of the coagulation cascade.

cause of FES [11].

**4. Incidence**

fractures [13–15].

Clinical presentation of the fat embolism syndrome starts with hypoxia, abnormalities in the neurological status, as well as development of petechiae that can be found in the region of the head, neck, and chest. Characteristic for development of petechiae is that they cannot be found in all patients, and some studies have shown their presentation in only 20–50% of cases. Also it is important to emphasize fever that follows the clinical presentation from the beginning. For the survival and adequate care of the patient, it is extremely important to recognize the development of fat embolism syndrome at the beginning. It is known that the development of this syndrome starts 1–2 days after the trauma in a period that can be referred to as a latent period. In some studies, the authors have concluded that fat embolism syndrome develops in the first 24 h (in around 60% of all cases), while in the rest of the traumatized patients, it can be recognized in the first 72 h.

For the proper understanding and better and faster diagnosis of fat embolism syndrome, Gurd and Wilson have developed a classification of the symptoms, where they have divided all symptoms in major or minor signs [16]. For diagnosing a fat embolism syndrome, it is necessary to notice one major and four minor signs that are shown in **Table 1**.

Nowadays, some authors in their studies have noticed the rigidity of the criteria mentioned above. In the study done by Lindeque and colleagues, development of the fat embolism syndrome was noticed with following signs: (1) pCO<sup>2</sup> of more than 55 mg Hg or pH of less than 7.3, (2) sustained respiratory rate of more than 35 breaths/min, and (3) dyspnea, tachycardia, and anxiety which they have suggested to be added in the criteria of Gurd and Wilson [17].

#### **5.1. Major signs of FES**

Hypoxia – even though pulmonary symptoms can be developed in a traumatized patient by the pulmonary embolism, heart failure, aspiration, or medication reaction, when none of the mentioned pathogenesis can be connected with patient's clinical presentation, fat embolism syndrome must be suspected in differential diagnosis. For a patient, it is very important to be on an oxygen support from the time of admittance in a hospital.


**Table 1.** Major and minor signs of fat embolism syndrome.

Neurological status – in order to be monitored on a proper way, a full neurological status must be examined from the time of admittance of a patient. Every deviation in neurological status must be a suspicion on the development of FES. By the studies published so far on this topic, it is noted that in around 80% of patients with FES, some alterations in neurological status have been noticed. It is also of great importance to exclude the factors that can lead to changes in neurological status and that are not connected with FES (hypoxia, head trauma, etc.). Alterations of consciousness or seizures are considered as a bad prognostic sign.

Petechiae – as mentioned before, not all patients with developed fat embolism syndrome have petechiae as a major sign. They are presented in 20–50% of patients with FES, and their distribution can affect not only the head, neck, and anterior aspect of chest but also the axillar region, palate, and conjunctivae and are caused by embolic fat.

#### **6. Treatment options and prevention**

There is no strict protocol regarding possible prevention of fat embolism syndrome. It is considered that immobilization of long bone fracture, fast transport to the hospital unit, and immediate stabilization of the fracture can be ways to prevent the development of fat embolism syndrome. Also, fluid compensation and oxygen support from the moment of admittance into the hospital also reduce the risk of development of FES. It is known that oxygen support has value in prevention of FES.

In order to properly follow up the patient's condition regarding development of FES, it is recommended to daily monitor blood pressure, complete blood count, blood gas values, diuresis, and arterial oxygen on room air together with daily clinical examination.

From the moment of admittance into the hospital, increased fluid compensation (saline, Ringer solution, or hypertonic glucose) and low-molecular-weight heparin or acetylsalicylic acid are measures that possibly prevent the development of fat embolism syndrome [18].

Some studies have shown efficiency in preventing FES by giving large doses of corticosteroids immediately after the injury.

#### **Author details**

Ismet Gavrankapetanović<sup>1</sup> \*, Adnan Papović<sup>1</sup> , Mehmed Jamakosmanović<sup>1</sup> , Elvir Baždar<sup>1</sup> and Lejla Tafro2

\*Address all correspondence to: ismetcap@ortotrauma.com.ba

1 Clinic for Orthopedics and Traumatology, University Clinical Center Sarajevo, Sarajevo, Bosnia and Herzegovina

2 Clinic for Anesthesiology, University Clinical Center Sarajevo, Sarajevo, Bosnia and Herzegovina

#### **References**

Neurological status – in order to be monitored on a proper way, a full neurological status must be examined from the time of admittance of a patient. Every deviation in neurological status must be a suspicion on the development of FES. By the studies published so far on this topic, it is noted that in around 80% of patients with FES, some alterations in neurological status have been noticed. It is also of great importance to exclude the factors that can lead to changes in neurological status and that are not connected with FES (hypoxia, head trauma, etc.). Alterations of consciousness or seizures are considered as a bad prognostic

Petechiae – as mentioned before, not all patients with developed fat embolism syndrome have petechiae as a major sign. They are presented in 20–50% of patients with FES, and their distribution can affect not only the head, neck, and anterior aspect of chest but also the axillar

There is no strict protocol regarding possible prevention of fat embolism syndrome. It is considered that immobilization of long bone fracture, fast transport to the hospital unit, and immediate stabilization of the fracture can be ways to prevent the development of fat embolism syndrome. Also, fluid compensation and oxygen support from the moment of admittance into the hospital also reduce the risk of development of FES. It is known that oxygen

In order to properly follow up the patient's condition regarding development of FES, it is recommended to daily monitor blood pressure, complete blood count, blood gas values, diure-

From the moment of admittance into the hospital, increased fluid compensation (saline, Ringer solution, or hypertonic glucose) and low-molecular-weight heparin or acetylsalicylic acid are measures that possibly prevent the development of fat embolism syndrome [18].

Some studies have shown efficiency in preventing FES by giving large doses of corticosteroids

1 Clinic for Orthopedics and Traumatology, University Clinical Center Sarajevo, Sarajevo,

2 Clinic for Anesthesiology, University Clinical Center Sarajevo, Sarajevo, Bosnia and

, Mehmed Jamakosmanović<sup>1</sup>

, Elvir Baždar<sup>1</sup>

and

sis, and arterial oxygen on room air together with daily clinical examination.

\*, Adnan Papović<sup>1</sup>

\*Address all correspondence to: ismetcap@ortotrauma.com.ba

region, palate, and conjunctivae and are caused by embolic fat.

**6. Treatment options and prevention**

98 Embolic Diseases - Unusual Therapies and Challenges

support has value in prevention of FES.

immediately after the injury.

Ismet Gavrankapetanović<sup>1</sup>

Bosnia and Herzegovina

**Author details**

Lejla Tafro2

Herzegovina

sign.


#### **Chapter 8**

### **Air Embolism**

#### Bojan Biocina, Mate Petricevic and Ivica Safradin

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.68649

#### **Abstract**

Air embolism is one of the serious causes of morbidity and mortality in medicine and surgery, especially in cardiac surgery. Various medical and surgical procedures have been associated with the risk of air embolism. In the chapter, all procedures and pathologic conditions will be described, paying special attention to the root cause analysis of the events in any given circumstance. Special attention is to be paid to techniques of risk minimization of this serious complication. The chapter will give an in-depth insight to the anatomical, physiological and other preconditions of air embolism, thus helping the reader to implement preventive measures and to increase patient safety

**Keywords:** embolism, air, gas

#### **1. Introduction**

Air embolism is, although uncommon, a potentially catastrophic event that occurs as a consequence of the entry of air into either arteries or veins. Put briefly, air embolism occurs when atmospheric gas is introduced into the systemic vasculature. Here, it would be prudent to clarify that the most appropriate name for this entity would actually be "gas embolism". In most cases, gas embolism is in fact air embolism, although the medical use of other gases such as carbon dioxide, nitrous oxide and nitrogen can also result in the condition [1].

Air embolism in the vasculature is the clinical entity with the great potential for severe morbidity and mortality. Venous air embolism is more prevalent when compared to arterial gas embolism. Even though the etiology of air embolism will be discussed in more detail later on, it is worth to mention that air embolism is actually predominantly an iatrogenic complication of both diagnostic and therapeutic procedures in different medical specialties [1–6].

© 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

#### **2. Etiology**

As previously mentioned, gas embolism can be either venous or arterial. The most common causes of air embolism are surgery, trauma, vascular interventions and barotrauma from mechanical ventilation and diving [7–10].

Gas embolism most commonly occurs not only in an anterograde venous course, as is most typical, but also may occur via epidural spaces and/or via tissue planes [2]. Medical specialties with documented cases of gas embolism were comprehensively reviewed by Muth et al. [1]. According to the literature, gas embolism may occur in cardiac surgery, cardiology, critical care and pulmonology, diving and hyperbaric medicine, endoscopic and laparoscopic surgery, gastroenterology, nephrology, neurosurgery, obstetrics and gynecology, otolaryngology, orthopedics, urology, vascular surgery, etc. [9–23]. Among these, air embolism occurs more frequently in neurosurgical and otolaryngological procedures when compared to surgical procedures in other specialties. An air embolism incident during neurosurgical procedures ranges from 10 to 80%.

There are numerous surgical or other non-surgical invasive procedures where gas embolism has been reported as a complication: (1) needle biopsy of the lung (bronchoscopic or percutaneous), lung resection [15–17, 24] and radiofrequency ablation of lung cancer [25], (2) arthroscopy and arthroplasty [18, 26], (3) gynecological procedures (hysteroscopy [19, 27, 28], C-section [29]), (4) gastrointestinal procedures (laparoscopy [30], colonoscopy [21], endoscopic retrograde cholangiopancreatography (ERCP) [20]) and (5) cardiac procedures (heart surgeries performed with cardiopulmonary bypass [22], cardiac implantable electronic devices implantation [23, 31], cardiac ablation procedures of cardiac arrhythmias) [32–34]. Gas embolism has also been described in ophthalmological [35] and dental procedures [36]. Mechanisms for gas embolism differ widely among the specialties. For example, in cardiac surgery procedures, possible mechanisms are the entry of air into extracorporeal bypass pump circuit and incomplete removal of air from the heart following weaning from cardiopulmonary bypass [22]. In neurosurgery procedures, the possible mechanism of gas embolism is entry of air through incised veins and calvarial bone, especially during craniotomy with the patient in a sitting position. What remains common for all the surgical procedures is the intraoperative use of hydrogen peroxide which may cause formation of arterial and venous oxygen emboli [1].

Gas embolism may certainly occur when handling intravascular catheters. Gas emboli can occur at the time of catheter insertion, while catheter is in place, or at the time of catheter removal [37]. Handling different types of catheters, be it venous or arterial (i.e., central venous catheters [10, 38], hemodialysis catheters [39, 40], pulmonary artery catheters [41] and angioplasty catheters [42]) may result in gas embolism. When handling intravascular catheters, one should keep in mind the factors that contribute to gas embolism occurrence (fracture or detachment of catheter connections, failure to occlude the needle hub, dysfunction of selfsealing valves in plastic introducer sheaths, the presence of a persistent catheter tract following the catheter removal, deep inspiration during catheter insertion or removal, hypovolemia that reduces central venous pressure and upright positioning of the patient).

#### **3. Detection of gas embolism**

**2. Etiology**

ranges from 10 to 80%.

mechanical ventilation and diving [7–10].

102 Embolic Diseases - Unusual Therapies and Challenges

As previously mentioned, gas embolism can be either venous or arterial. The most common causes of air embolism are surgery, trauma, vascular interventions and barotrauma from

Gas embolism most commonly occurs not only in an anterograde venous course, as is most typical, but also may occur via epidural spaces and/or via tissue planes [2]. Medical specialties with documented cases of gas embolism were comprehensively reviewed by Muth et al. [1]. According to the literature, gas embolism may occur in cardiac surgery, cardiology, critical care and pulmonology, diving and hyperbaric medicine, endoscopic and laparoscopic surgery, gastroenterology, nephrology, neurosurgery, obstetrics and gynecology, otolaryngology, orthopedics, urology, vascular surgery, etc. [9–23]. Among these, air embolism occurs more frequently in neurosurgical and otolaryngological procedures when compared to surgical procedures in other specialties. An air embolism incident during neurosurgical procedures

There are numerous surgical or other non-surgical invasive procedures where gas embolism has been reported as a complication: (1) needle biopsy of the lung (bronchoscopic or percutaneous), lung resection [15–17, 24] and radiofrequency ablation of lung cancer [25], (2) arthroscopy and arthroplasty [18, 26], (3) gynecological procedures (hysteroscopy [19, 27, 28], C-section [29]), (4) gastrointestinal procedures (laparoscopy [30], colonoscopy [21], endoscopic retrograde cholangiopancreatography (ERCP) [20]) and (5) cardiac procedures (heart surgeries performed with cardiopulmonary bypass [22], cardiac implantable electronic devices implantation [23, 31], cardiac ablation procedures of cardiac arrhythmias) [32–34]. Gas embolism has also been described in ophthalmological [35] and dental procedures [36]. Mechanisms for gas embolism differ widely among the specialties. For example, in cardiac surgery procedures, possible mechanisms are the entry of air into extracorporeal bypass pump circuit and incomplete removal of air from the heart following weaning from cardiopulmonary bypass [22]. In neurosurgery procedures, the possible mechanism of gas embolism is entry of air through incised veins and calvarial bone, especially during craniotomy with the patient in a sitting position. What remains common for all the surgical procedures is the intraoperative use of hydrogen peroxide which may

Gas embolism may certainly occur when handling intravascular catheters. Gas emboli can occur at the time of catheter insertion, while catheter is in place, or at the time of catheter removal [37]. Handling different types of catheters, be it venous or arterial (i.e., central venous catheters [10, 38], hemodialysis catheters [39, 40], pulmonary artery catheters [41] and angioplasty catheters [42]) may result in gas embolism. When handling intravascular catheters, one should keep in mind the factors that contribute to gas embolism occurrence (fracture or detachment of catheter connections, failure to occlude the needle hub, dysfunction of selfsealing valves in plastic introducer sheaths, the presence of a persistent catheter tract following the catheter removal, deep inspiration during catheter insertion or removal, hypovolemia

that reduces central venous pressure and upright positioning of the patient).

cause formation of arterial and venous oxygen emboli [1].

In order to diagnose air embolism, a clinician should first set the suspicion and should assess clinical findings. Many cases of gas embolism are subclinical with no adverse outcomes. Usually, even when symptoms are present, they are non-specific, and a high index of clinical suspicion for possible gas embolism is required to prompt investigations and initiate appropriate therapy. A splashing auscultatory sign indicating the presence of gas in cardiac chambers can be auscultated using stethoscope [1]. Doppler ultrasonography is a sensitive and a practical means of detecting intracardiac air [43, 44]. Transesophageal echocardiography remains an even more sensitive and definitive method for detecting intracardiac gas [45].

Transesophageal echocardiography is currently the most sensitive monitoring device for detection of air presence, detecting as little as 0.02 ml/kg of air administered by bolus injection [46, 47]. The major deterrents to transesophageal echocardiography are that it is invasive, is expensive and requires expertise and constant vigilance that may limit its use to just a welltrained cardiac anesthesiologist or cardiologist [2].

Noteworthy, a decrease in the end-tidal carbon dioxide levels, as determined by capnometry, may be suggestive of gas embolism as well.

#### **4. Management**

Early diagnosis and treatment before catastrophic cardiovascular collapse are of utmost importance. In general, there are three principle goals in air embolism management: (1) prevention of further air entry, (2) a reduction in the volume of air entrapped and (3) hemodynamic support [2]. In case of gas embolism, clinician should institute high-flow oxygen to maximize patient oxygenation during the period of hemodynamic instability. Nitrous oxide should be discontinued, and the patient should be placed on 100% oxygen. Administration of oxygen is important not only to treat hypoxia and hypoxemia but also to eliminate the gas in the bubbles by establishing a diffusion gradient that favors the egress of gas from bubbles [1, 48]. In certain cases, therapy with catecholamines is required, as well as aggressive cardiopulmonary resuscitation, if needed. Rapid volume expansion is recommended to elevate venous pressure, thus preventing the continued entry of gas into intravascular space. Normovolemia should be achieved to optimize microcirculation. Colloid solutions are preferable to crystalloid solutions for hemodilution as crystalloid solutions may promote cerebral edema.

Hyperbaric oxygen therapy decreases the size of the gas bubble both by rising the ambient pressure and by causing hyperoxia [1]. There is emerging evidence suggesting that all patients with clinical symptoms of arterial gas embolism should receive recompression treatment with hyperbaric oxygen, which is in fact considered the first line treatment of choice for arterial gas embolism [1, 49–51].

As Muth et al. discussed in their paper [1], there is evidence that heparin may be beneficial in the treatment of gas embolism [52]. The possible disadvantage would be the risk of hemorrhage into the infarcted tissue. Whereas the use of corticosteroid therapy remains controversial and to date is not recommended, the lidocaine therapy has been shown to provide cerebral protection during cardiac surgery [53]. Even with lidocaine, the evidence is controversial [1, 54] and further research is needed to shed a light into its neuroprotective role.

In conclusion, gas embolism is a risk associated with different diagnostic and/or therapeutic procedures in virtually all medical specialties [1]. Arterial gas emboli may be particularly dangerous if they occlude cardiac or cerebral vessels [1]. Whereas hyperbaric oxygen remains the first choice of arteria gas emboli treatment, the mainstays of treatment for venous gas embolism are volume expansion, targeting 12 mm of mercury of central venous pressure, the administration of 100% oxygen, often with ventilatory support [1]. Finally, prevention of air embolism and prevention of further entry of gas in cases of present air embolism remain the Cornerstone Treatment in management of patients at risk for such a clinical entity.

#### **Author details**

Bojan Biocina<sup>1</sup> \*, Mate Petricevic<sup>2</sup> and Ivica Safradin2


#### **References**


[7] Dudney TM, Elliott CG. Pulmonary embolism from amniotic fluid, fat, and air. Progress in Cardiovascular Diseases. 1994;**36**:447-474

into the infarcted tissue. Whereas the use of corticosteroid therapy remains controversial and to date is not recommended, the lidocaine therapy has been shown to provide cerebral protection during cardiac surgery [53]. Even with lidocaine, the evidence is controversial [1, 54] and

In conclusion, gas embolism is a risk associated with different diagnostic and/or therapeutic procedures in virtually all medical specialties [1]. Arterial gas emboli may be particularly dangerous if they occlude cardiac or cerebral vessels [1]. Whereas hyperbaric oxygen remains the first choice of arteria gas emboli treatment, the mainstays of treatment for venous gas embolism are volume expansion, targeting 12 mm of mercury of central venous pressure, the administration of 100% oxygen, often with ventilatory support [1]. Finally, prevention of air embolism and prevention of further entry of gas in cases of present air embolism remain the

Cornerstone Treatment in management of patients at risk for such a clinical entity.

and Ivica Safradin2

1 Department of Cardiac Surgery, School of Medicine, University of Zagreb, Zagreb, Croatia

[1] Muth CM, Shank ES. Gas embolism. The New England Journal of Medicine. 2000;**342**:

[2] Mirski MA, Lele AV, Fitzsimmons L, Toung TJ. Diagnosis and treatment of vascular air

[3] Sviri S, Woods WP, van Heerden PV. Air embolism – A case series and review. Critical Care and Resuscitation: Journal of the Australasian Academy of Critical Care Medicine.

[4] van Hulst RA, Klein J, Lachmann B. Gas embolism: Pathophysiology and treatment.

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further research is needed to shed a light into its neuroprotective role.

**Author details**

\*, Mate Petricevic<sup>2</sup>

104 Embolic Diseases - Unusual Therapies and Challenges

\*Address all correspondence to: bbiocina@kbc-zagreb.hr

embolism. Anesthesiology. 2007;**106**:164-77

2 Department of Cardiac Surgery, UHC Zagreb, Zagreb, Croatia

Bojan Biocina<sup>1</sup>

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