Can J Anesth/J Can Anesth DOI 10.1007/s12630-014-0137-6
SPECIAL ARTICLE
From the Journal archives: Pulmonary marrow embolism: lessons learned from a canine model simulating dual component cemented arthroplasty Stephen Kowalski, MD • Dean Bell, MD Brad Pilkey, MD
•
Received: 15 November 2013 / Accepted: 3 March 2014 Ó Canadian Anesthesiologists’ Society 2014
Article Summary Editors’ Note: Classics Revisited Key Articles from the Canadian Journal of Anesthesia Archives: 1954-2013 As part of the Journal’s 60th anniversary Diamond Jubilee Celebration, a number of seminal articles from the Journal archives are highlighted in the Journal’s 61st printed volume and online at: www.springer.com/12630. The following article was selected on the basis of its novelty at the time of publication, its scientific merit, and its overall importance to clinical practice: Byrick RJ, Kay JC, Mullen JBM. Pulmonary marrow embolism: a dog model simulating dual component cemented arthroplasty. Can J Anaesth 1987; 34: 336-42. Herein, Dr. Stephen Kowalski and his colleagues provide expert commentary on this key article, one of a series of important studies by this group elucidating the systemic cardiovascular and histologic responses that occur during cemented hip arthroplasty. Hilary P. Grocott MD, Editor-in-Chief Donald R. Miller MD, Former Editor-in-Chief
S. Kowalski, MD D. Bell, MD Department of Anesthesia and Perioperative Medicine, University of Manitoba, Winnipeg, MB, Canada B. Pilkey, MD Department of Surgery, Section of Orthopedics, University of Manitoba, Winnipeg, MB, Canada S. Kowalski, MD (&) Department of Anesthesia, Health Sciences Centre, University of Manitoba, AE210 671 William Avenue, Winnipeg, MB R3E 0Z2, Canada e-mail: [email protected]
A canine model of cemented arthroplasty was used to assess the hemodynamic and gas exchange abnormalities in bilateral cemented prostheses as compared with unilateral prosthesis. The animals were anesthetized and their lungs were mechanically ventilated. Cardiovascular monitoring was achieved with an arterial catheter, a thermodilution pulmonary artery catheter, and a left atrial catheter. The distal femur was exposed and the femoral canal was drilled and reamed. Bone cement and a metal prostheses were then inserted. Serial cardiac output measurements and arterial, mixed venous, and mixed expiratory gas values were then taken at five, 15, 30, and 60 min following prosthesis insertion. All pressures were measured continuously. Intrapulmonary shunt (Qs/Qt) and dead space to tidal volume ratio (Vd/Vt) were calculated using standard equations. After 60 min, the animals were euthanized and the lungs were inflated, removed en bloc, and fixed in formalin. The lungs were subsequently processed for histological examination with 5-lm thick slices. Morphometric measurements were performed on six sample lung specimens from each dog, and the number of fat emboli was calculated from 12 random fields from each of the lung segments. Statistical analysis was performed using Student’s t test, two-way analysis of variance, and Dunnett’s multiple range test where applicable. Authors: Byrick RJ, Kay JC, Mullen JBM. Citation: Can J Anaesth 1987; 34: 336-42. Purpose: The purpose of this study was to evaluate the cardiopulmonary changes in a canine model resulting from insertion of bilateral, cemented, femoral prostheses as compared with a unilateral cemented prosthesis. Principal findings: There was a greater decrease in systemic blood pressure and a larger increase in pulmonary artery
123
S. Kowalski et al.
pressure and pulmonary vascular resistance with bilateral cemented prostheses as compared with a unilateral cemented prosthesis. Nevertheless, there were no differences between groups in either cardiac index or left atrial pressures (Fig. 1). Cardiac output decreased in both groups with prosthesis insertion (Fig. 2). The study also showed a greater decrease in both arterial oxygenation and mixed venous oxygen tension with bilateral cemented prostheses as compared with unilateral prosthesis. Finally, histological examination showed that 25% of the pulmonary capillary bed was occluded by fat in the bilateral arthroplasty group. Conclusions: The larger embolic load with bilateral cemented prostheses as compared with unilateral prosthesis caused greater hemodynamic alterations and decreases in oxygenation. Early changes in hemodynamic variables and oxygenation are correlated with mechanical obstruction of the pulmonary circulation and not with significant acute pulmonary edema or inflammation.
Commentary Fat embolism syndrome was initially described in 1873. There were published reports describing a clinical triad of symptoms consisting of hypoxemia, neurological abnormalities, and petechial rash that complicated orthopedic injuries, specifically, long bone fractures. It was recognized that blood from patients was lipemic, and it was speculated that, when fractures occur, fat from bone marrow could enter the circulation and give rise to this syndrome. Fat embolism syndrome can occasionally develop with clinical conditions such as pancreatitis, burns, alcoholic (fatty) liver disease, and sickle cell hemoglobinopathies. Nevertheless, fat embolism syndrome occurs overwhelmingly with orthopedic trauma, especially long bone fractures,1 and is more common in closed fractures than in open fractures. A single long bone fracture has an incidence of fat embolism of 1-3%, and the incidence will increase with the number of fractures. In patients with bilateral femoral fractures, the incidence of fat embolism has been reported as high as 33%.2 Fat embolism syndrome typically develops within 24-72 hr following long bone fracture. Respiratory symptoms are the most common and can manifest as hypoxemia, tachypnea, and dyspnea. The most severe forms can develop a fulminant acute respiratory distress syndrome requiring mechanical ventilation. Neurological symptoms are nonspecific and consist of confusion, drowsiness, and occasionally seizures. A petechial rash is the least commonly observed symptom. In the perioperative period, fat embolism can sometimes have a
123
Fig. 1 Mean (± SEM) values for arterial blood pressure (BP), pulmonary artery pressure (PAP) and left atrial pressure (LAP) prior to cement and prosthesis insertion (C) and at five, 15, 30 and 60 min after arthroplasty procedure in each group. *Indicates statistically significant difference from control (C) value. Reproduced with permission from: Byrick RJ, Kay JC, Mullen JB. Pulmonary marrow embolism: a dog model simulating dual component cemented arthroplasty. Can J Anaesth 1987; 34: 336-42
sudden and fulminant presentation with severe hypoxemia and cardiovascular collapse from acute right ventricular failure.3 The pathophysiology of fat embolism syndrome is multifactorial. There is a component related to the mechanical embolic load of fat, with emboli coalescing and forming thrombotic masses, which may cause sudden cardiac collapse in susceptible patients. There is also a biochemical/inflammatory component contributing to the clinical syndrome. Neutral fats are the major constituent of bone marrow and do not initiate an inflammatory response; however, free fatty acids are known to cause severe vasculitis and hemorrhagic pulmonary edema in animal models. Over time, neutral fats can be hydrolyzed to free
Key article from the journal archives
Fig. 2 Mean (± SEM) values of cardiac output and calculated pulmonary vascular resistance (PVR) prior to cement and prosthesis insertion (C) and at five-, 15-, 30- and 60-min intervals after arthroplasty procedure in each group. *Indicates statistically significant difference from control (C) value. Reproduced with permission from: Byrick RJ, Kay JC, Mullen JB. Pulmonary marrow embolism: a dog model simulating dual component cemented arthroplasty. Can J Anaesth 1987; 34: 336-42
fatty acids, which may account for the subacute clinical presentation of fat embolism syndrome.3 A variety of biochemical mediators, such as platelet-activating factor, thromboxane A2, cyclic guanosine monophosphate, serotonin, and nitric oxide, are released and may contribute to a systemic inflammatory response.4 Platelet activation has been shown to occur after bone marrow pressurization and intravasation of marrow contents. This can stimulate intravascular coagulation as well as release of vasoactive substances and contribute to a rise in pulmonary artery pressure.5 In addition, fat can be found in the arterial circulation of patients. It may pass from the right to the left side of the circulation if there is a patent foramen ovale accompanied by an acute rise in right-sided pressures. Liquid fat can also pass directly through the pulmonary circulation and has been found in cerebral microvessels (possibly accounting for changes in the central nervous system CNS) and in the skin of patients, associated with petechial changes.6,7 The treatment of fat embolism syndrome is largely supportive, consisting of maintaining oxygenation and ventilation and providing circulatory support.
Corticosteroids have been used to treat the syndrome, but use of these drugs is controversial and has not been shown to have a mortality benefit.2,3 The single most important intervention is early stabilization of long bone fractures with operative fixation, for which these patients will frequently present.8 The incidence of fat embolism has been reported anywhere from 0.9-35% of patients depending on the specific population studied. Notably, it is a consistent finding that the incidence of fat embolism is higher on postmortem diagnosis than on clinical diagnosis.9 More recently, with the advent of transesophageal echocardiography, it has been recognized that embolization of bone marrow contents is a common occurrence. In some reports, up to 87% of patients with long bone fractures will have evidence of embolization during intraoperative fixation of the fracture.10 The occurrence of fat embolization is common, but the development of clinically significant fat embolism syndrome is rare. Modern total hip arthroplasties started in 1961, and total knee arthroplasty dates to 1972. Currently, over 300,000 hip arthroplasties and 600,000 knee arthroplasties are performed on an annual basis in the United States.11 Throughout the 1970s and early 1980s, there were reports of hypotension, cardiac arrest, and death in the minutes following cement and prosthesis insertion.12,13 Importantly, and the focus of this commentary, Byrick et al. from St. Michael’s Hospital at the University of Toronto developed a dog model to study various facets of bone marrow embolism.14 They have continued to investigate the pathophysiological factors associated with marrow embolism and have 34 articles published on the topic from 1983-2013. During the 1983-1987 period, Byrick’s group specifically assessed the role of medullary canal lavage,14 the impact of insertion of bilateral cemented arthroplasties vs insertion of a unilateral cemented arthroplasty,13 and the impact of using cement when performing arthroplasty.15 Their most cited paper (with more than 130 citations), published in 1987, showed that pressurizing bone cement caused pulmonary microemboli and cardiopulmonary dysfunction.16 Their article, published in the Journal in 1987, established that bilateral cemented arthroplasty is associated with greater changes in oxygenation, blood pressure, and pulmonary vascular resistance.13 This article showed that the extent and degree of embolic load to the lungs would affect the physiological response. Subsequent studies have also shown evidence of platelet activation and stimulation of the coagulation cascade, which can further contribute to the biochemical insult with marrow embolism. Simply put, the greater the embolic load, the greater the chance for adverse complications.
123
S. Kowalski et al.
The current standard of care for long bone fractures involves early fixation and stabilization, however, only a minority of patients will develop the potentially lifethreatening complications. The question as to which patient(s) will develop problems is clearly multifactorial and dependent on the patient’s baseline medical condition, comorbidities, and associated injuries (e.g., aspiration, infection, etc.), but the embolic load is a clinically significant and potentially modifiable factor. There may be certain risk factors present that can place patients at risk for fat embolism syndrome. Respiratory distress can result from a ‘‘second hit’’ of fat emboli to a previous pulmonary injury, e.g., a patient with a femur fracture and pulmonary contusion. The use of damage control surgery with emergent external fixation avoids causing an acute secondary hit to the pulmonary system. Alternatively, fat emboli may also overload a seemingly normal pulmonary system in patients with metastatic disease.11 Patterson et al.13 identified four risk factors associated with cardiorespiratory dysfunction when performing cemented hip arthroplasty with long stem components. Common to all patients were: advanced age, osteoporotic bone, a previously undisturbed medullary canal, and use of a long stem component with several batches of cement. Prevention strategies can be employed to decrease the marrow load that is released during these procedures. Pulsatile lavage and thorough suction of the medullary canal can reduce the embolic response seen on transesophageal echocardiography. Vent holes into the medullary canal may reduce the embolic load. Vent holes in anatomic specimen models can reduce the intramedullary pressure, though the technique has not been verified in clinical practice. Additionally, there are concerns about cement seeping through the vent holes, potentially damaging the soft tissues or weakening the cement mantle. Pitto et al.17 described a bone-vacuum technique to limit fat embolism during cemented hip arthroplasty. Three techniques were compared: uncemented, conventional cemented, and bone-vacuum cemented arthroplasties. No embolic events occurred in the uncemented group. Hypotension, arterial oxygen desaturation, and increased pulmonary shunting were significant in the conventional technique, but no changes occurred in these parameters in the uncemented and bone-vacuum techniques. It is most prudent to avoid cementing in patients who cannot tolerate a significant increase in pulmonary shunting. If cementing is required due to poor bone stock, meticulous care should be taken to irrigate and aspirate the intramedullary canal before cement insertion. Recently, there has been a move towards using more uncemented short and long stem components in patients with low pulmonary reserve as adverse cardiopulmonary events have not been reported with these implants.
123
Management of the high-risk patient for either elective or trauma surgery mandates good communication and planning between the orthopedic surgeon and anesthesiologist. As previously stated, fat embolism syndrome, although more common in trauma than in elective procedures, has become a relatively rare occurrence. A recent review from Taiwan reported an incidence of 2.4% in patients with multiple fractures and less than 1% in patients with only a single fracture.18 The current safety of these treatments in both elective and trauma cases is due, in large part, to basic bench research by clinician scientists such as Robert Byrick, and reported here in the Journal. Funding sources
None.
Conflicts of interest
None declared.
References 1. Mellor A, Soni N. Fat embolism. Anaesthesia 2001; 56: 145-54. 2. Johnson MJ, Lucas GL. Fat embolism syndrome. Orthopedics 1996; 19: 41-8. 3. Nixon JR, Brock-Utne JG. Free fatty acid and arterial oxygen changes following major injury: a correlation between hypoxemia and increased free fatty acid levels. J Trauma 1978; 18: 23-6. 4. Akhtar S. Fat embolism. Anesthesiol Clin 2009; 27: 533-50. 5. Blankstein M, Byrick RJ, Nakane M, et al. A preliminary study of platelet activation after embolization of marrow contents. J Orthop Trauma 2012; 26: e214-20. 6. Sulek CA, Davies LK, Enneking FK, Gearen PA, Lobato EB. Cerebral microembolism diagnosed by transcranial Doppler during total knee arthroplasty: correlation with transesophageal echocardiography. Anesthesiology 1999; 91: 672-6. 7. Byrick RJ, Kay JC, Mazer CD, Wang Z, Mullen JB. Dynamic characteristics of cerebral lipid microemboli: videomicroscopy studies in rats. Anesth Analg 2003; 97: 1789-94. 8. Riska EB, Myllynen P. Fat embolism in patients with multiple injuries. J Trauma 1982; 22: 891-4. 9. Eriksson EA, Pellegrini DC, Vanderkolk WE, Minshall CT, Fakhry SM, Cohle SD. Incidence of pulmonary fat embolism at autopsy: an undiagnosed epidemic. J Trauma 2011; 71: 312-5. 10. Christie J, Robinson CM, Pell AC, McBirnie J, Burnett R. Transcardiac echocardiography during invasive intramedullary procedures. J Bone Joint Surg Br 1995; 77: 450-5. 11. Issack PS, Lauerman MH, Helfet DL, Sculco TP, Lane JM. Fat embolism and respiratory distress associated with cemented femoral arthroplasty. Am J Orthop (Belle Mead NJ) 2009; 38: 72-6. 12. Byrick RJ, Forbes D, Waddell JP. A monitored cardiovascular collapse during cemented total knee replacement. Anesthesiology 1986; 65: 213-6. 13. Patterson BM, Healey JH, Cornell CN, Sharrock NE. Cardiac arrest during hip arthroplasty with a cemented long-stem component. A report of seven cases. J Bone Joint Surg Am 1991; 73: 271-7. 14. Byrick RJ, Kay JC, Mullen JB. Pulmonary marrow embolism: a dog model simulating dual component cemented arthroplasty. Can J Anaesth 1987; 34: 336-42. 15. Sherman RM, Byrick RJ, Kay JC, Sullivan TR, Waddell JP. The role of lavage in preventing hemodynamic and blood-gas changes during cemented arthroplasty. J Bone Joint Surg Am 1983; 65: 500-6.
Key article from the journal archives 16. Orsini EC, Byrick RJ, Mullen BM, Kay JC, Waddell JP. Cardiopulmonary function and pulmonary microemboli during arthroplasty using cemented or non-cemented components. The role of intramedullary pressure. J Bone Joint Surg Am 1987; 69: 822-32. 17. Pitto RP, Koessler M, Kuehle JW. Comparison of fixation of the femoral component without cement and fixation with use of a bone-
vacuum cementing technique for the prevention of fat embolism during total hip arthroplasty. A prospective, randomized clinical trial. J Bone Joint Surg Am 1999; 81: 831-43. 18. Tsai IT, Hsu CJ, Chen YH, Fong YC, Hsu HC, Tsai CH. Fat embolism syndrome in long bone fracture—clinical experience in a tertiary referral center in Taiwan. J Chin Med Assoc 2010; 73: 407-10.
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SPECIAL ARTICLE
From the Journal archives: Pulmonary marrow embolism: lessons learned from a canine model simulating dual component cemented arthroplasty Stephen Kowalski, MD • Dean Bell, MD Brad Pilkey, MD
•
Received: 15 November 2013 / Accepted: 3 March 2014 Ó Canadian Anesthesiologists’ Society 2014
Article Summary Editors’ Note: Classics Revisited Key Articles from the Canadian Journal of Anesthesia Archives: 1954-2013 As part of the Journal’s 60th anniversary Diamond Jubilee Celebration, a number of seminal articles from the Journal archives are highlighted in the Journal’s 61st printed volume and online at: www.springer.com/12630. The following article was selected on the basis of its novelty at the time of publication, its scientific merit, and its overall importance to clinical practice: Byrick RJ, Kay JC, Mullen JBM. Pulmonary marrow embolism: a dog model simulating dual component cemented arthroplasty. Can J Anaesth 1987; 34: 336-42. Herein, Dr. Stephen Kowalski and his colleagues provide expert commentary on this key article, one of a series of important studies by this group elucidating the systemic cardiovascular and histologic responses that occur during cemented hip arthroplasty. Hilary P. Grocott MD, Editor-in-Chief Donald R. Miller MD, Former Editor-in-Chief
S. Kowalski, MD D. Bell, MD Department of Anesthesia and Perioperative Medicine, University of Manitoba, Winnipeg, MB, Canada B. Pilkey, MD Department of Surgery, Section of Orthopedics, University of Manitoba, Winnipeg, MB, Canada S. Kowalski, MD (&) Department of Anesthesia, Health Sciences Centre, University of Manitoba, AE210 671 William Avenue, Winnipeg, MB R3E 0Z2, Canada e-mail: [email protected]
A canine model of cemented arthroplasty was used to assess the hemodynamic and gas exchange abnormalities in bilateral cemented prostheses as compared with unilateral prosthesis. The animals were anesthetized and their lungs were mechanically ventilated. Cardiovascular monitoring was achieved with an arterial catheter, a thermodilution pulmonary artery catheter, and a left atrial catheter. The distal femur was exposed and the femoral canal was drilled and reamed. Bone cement and a metal prostheses were then inserted. Serial cardiac output measurements and arterial, mixed venous, and mixed expiratory gas values were then taken at five, 15, 30, and 60 min following prosthesis insertion. All pressures were measured continuously. Intrapulmonary shunt (Qs/Qt) and dead space to tidal volume ratio (Vd/Vt) were calculated using standard equations. After 60 min, the animals were euthanized and the lungs were inflated, removed en bloc, and fixed in formalin. The lungs were subsequently processed for histological examination with 5-lm thick slices. Morphometric measurements were performed on six sample lung specimens from each dog, and the number of fat emboli was calculated from 12 random fields from each of the lung segments. Statistical analysis was performed using Student’s t test, two-way analysis of variance, and Dunnett’s multiple range test where applicable. Authors: Byrick RJ, Kay JC, Mullen JBM. Citation: Can J Anaesth 1987; 34: 336-42. Purpose: The purpose of this study was to evaluate the cardiopulmonary changes in a canine model resulting from insertion of bilateral, cemented, femoral prostheses as compared with a unilateral cemented prosthesis. Principal findings: There was a greater decrease in systemic blood pressure and a larger increase in pulmonary artery
123
S. Kowalski et al.
pressure and pulmonary vascular resistance with bilateral cemented prostheses as compared with a unilateral cemented prosthesis. Nevertheless, there were no differences between groups in either cardiac index or left atrial pressures (Fig. 1). Cardiac output decreased in both groups with prosthesis insertion (Fig. 2). The study also showed a greater decrease in both arterial oxygenation and mixed venous oxygen tension with bilateral cemented prostheses as compared with unilateral prosthesis. Finally, histological examination showed that 25% of the pulmonary capillary bed was occluded by fat in the bilateral arthroplasty group. Conclusions: The larger embolic load with bilateral cemented prostheses as compared with unilateral prosthesis caused greater hemodynamic alterations and decreases in oxygenation. Early changes in hemodynamic variables and oxygenation are correlated with mechanical obstruction of the pulmonary circulation and not with significant acute pulmonary edema or inflammation.
Commentary Fat embolism syndrome was initially described in 1873. There were published reports describing a clinical triad of symptoms consisting of hypoxemia, neurological abnormalities, and petechial rash that complicated orthopedic injuries, specifically, long bone fractures. It was recognized that blood from patients was lipemic, and it was speculated that, when fractures occur, fat from bone marrow could enter the circulation and give rise to this syndrome. Fat embolism syndrome can occasionally develop with clinical conditions such as pancreatitis, burns, alcoholic (fatty) liver disease, and sickle cell hemoglobinopathies. Nevertheless, fat embolism syndrome occurs overwhelmingly with orthopedic trauma, especially long bone fractures,1 and is more common in closed fractures than in open fractures. A single long bone fracture has an incidence of fat embolism of 1-3%, and the incidence will increase with the number of fractures. In patients with bilateral femoral fractures, the incidence of fat embolism has been reported as high as 33%.2 Fat embolism syndrome typically develops within 24-72 hr following long bone fracture. Respiratory symptoms are the most common and can manifest as hypoxemia, tachypnea, and dyspnea. The most severe forms can develop a fulminant acute respiratory distress syndrome requiring mechanical ventilation. Neurological symptoms are nonspecific and consist of confusion, drowsiness, and occasionally seizures. A petechial rash is the least commonly observed symptom. In the perioperative period, fat embolism can sometimes have a
123
Fig. 1 Mean (± SEM) values for arterial blood pressure (BP), pulmonary artery pressure (PAP) and left atrial pressure (LAP) prior to cement and prosthesis insertion (C) and at five, 15, 30 and 60 min after arthroplasty procedure in each group. *Indicates statistically significant difference from control (C) value. Reproduced with permission from: Byrick RJ, Kay JC, Mullen JB. Pulmonary marrow embolism: a dog model simulating dual component cemented arthroplasty. Can J Anaesth 1987; 34: 336-42
sudden and fulminant presentation with severe hypoxemia and cardiovascular collapse from acute right ventricular failure.3 The pathophysiology of fat embolism syndrome is multifactorial. There is a component related to the mechanical embolic load of fat, with emboli coalescing and forming thrombotic masses, which may cause sudden cardiac collapse in susceptible patients. There is also a biochemical/inflammatory component contributing to the clinical syndrome. Neutral fats are the major constituent of bone marrow and do not initiate an inflammatory response; however, free fatty acids are known to cause severe vasculitis and hemorrhagic pulmonary edema in animal models. Over time, neutral fats can be hydrolyzed to free
Key article from the journal archives
Fig. 2 Mean (± SEM) values of cardiac output and calculated pulmonary vascular resistance (PVR) prior to cement and prosthesis insertion (C) and at five-, 15-, 30- and 60-min intervals after arthroplasty procedure in each group. *Indicates statistically significant difference from control (C) value. Reproduced with permission from: Byrick RJ, Kay JC, Mullen JB. Pulmonary marrow embolism: a dog model simulating dual component cemented arthroplasty. Can J Anaesth 1987; 34: 336-42
fatty acids, which may account for the subacute clinical presentation of fat embolism syndrome.3 A variety of biochemical mediators, such as platelet-activating factor, thromboxane A2, cyclic guanosine monophosphate, serotonin, and nitric oxide, are released and may contribute to a systemic inflammatory response.4 Platelet activation has been shown to occur after bone marrow pressurization and intravasation of marrow contents. This can stimulate intravascular coagulation as well as release of vasoactive substances and contribute to a rise in pulmonary artery pressure.5 In addition, fat can be found in the arterial circulation of patients. It may pass from the right to the left side of the circulation if there is a patent foramen ovale accompanied by an acute rise in right-sided pressures. Liquid fat can also pass directly through the pulmonary circulation and has been found in cerebral microvessels (possibly accounting for changes in the central nervous system CNS) and in the skin of patients, associated with petechial changes.6,7 The treatment of fat embolism syndrome is largely supportive, consisting of maintaining oxygenation and ventilation and providing circulatory support.
Corticosteroids have been used to treat the syndrome, but use of these drugs is controversial and has not been shown to have a mortality benefit.2,3 The single most important intervention is early stabilization of long bone fractures with operative fixation, for which these patients will frequently present.8 The incidence of fat embolism has been reported anywhere from 0.9-35% of patients depending on the specific population studied. Notably, it is a consistent finding that the incidence of fat embolism is higher on postmortem diagnosis than on clinical diagnosis.9 More recently, with the advent of transesophageal echocardiography, it has been recognized that embolization of bone marrow contents is a common occurrence. In some reports, up to 87% of patients with long bone fractures will have evidence of embolization during intraoperative fixation of the fracture.10 The occurrence of fat embolization is common, but the development of clinically significant fat embolism syndrome is rare. Modern total hip arthroplasties started in 1961, and total knee arthroplasty dates to 1972. Currently, over 300,000 hip arthroplasties and 600,000 knee arthroplasties are performed on an annual basis in the United States.11 Throughout the 1970s and early 1980s, there were reports of hypotension, cardiac arrest, and death in the minutes following cement and prosthesis insertion.12,13 Importantly, and the focus of this commentary, Byrick et al. from St. Michael’s Hospital at the University of Toronto developed a dog model to study various facets of bone marrow embolism.14 They have continued to investigate the pathophysiological factors associated with marrow embolism and have 34 articles published on the topic from 1983-2013. During the 1983-1987 period, Byrick’s group specifically assessed the role of medullary canal lavage,14 the impact of insertion of bilateral cemented arthroplasties vs insertion of a unilateral cemented arthroplasty,13 and the impact of using cement when performing arthroplasty.15 Their most cited paper (with more than 130 citations), published in 1987, showed that pressurizing bone cement caused pulmonary microemboli and cardiopulmonary dysfunction.16 Their article, published in the Journal in 1987, established that bilateral cemented arthroplasty is associated with greater changes in oxygenation, blood pressure, and pulmonary vascular resistance.13 This article showed that the extent and degree of embolic load to the lungs would affect the physiological response. Subsequent studies have also shown evidence of platelet activation and stimulation of the coagulation cascade, which can further contribute to the biochemical insult with marrow embolism. Simply put, the greater the embolic load, the greater the chance for adverse complications.
123
S. Kowalski et al.
The current standard of care for long bone fractures involves early fixation and stabilization, however, only a minority of patients will develop the potentially lifethreatening complications. The question as to which patient(s) will develop problems is clearly multifactorial and dependent on the patient’s baseline medical condition, comorbidities, and associated injuries (e.g., aspiration, infection, etc.), but the embolic load is a clinically significant and potentially modifiable factor. There may be certain risk factors present that can place patients at risk for fat embolism syndrome. Respiratory distress can result from a ‘‘second hit’’ of fat emboli to a previous pulmonary injury, e.g., a patient with a femur fracture and pulmonary contusion. The use of damage control surgery with emergent external fixation avoids causing an acute secondary hit to the pulmonary system. Alternatively, fat emboli may also overload a seemingly normal pulmonary system in patients with metastatic disease.11 Patterson et al.13 identified four risk factors associated with cardiorespiratory dysfunction when performing cemented hip arthroplasty with long stem components. Common to all patients were: advanced age, osteoporotic bone, a previously undisturbed medullary canal, and use of a long stem component with several batches of cement. Prevention strategies can be employed to decrease the marrow load that is released during these procedures. Pulsatile lavage and thorough suction of the medullary canal can reduce the embolic response seen on transesophageal echocardiography. Vent holes into the medullary canal may reduce the embolic load. Vent holes in anatomic specimen models can reduce the intramedullary pressure, though the technique has not been verified in clinical practice. Additionally, there are concerns about cement seeping through the vent holes, potentially damaging the soft tissues or weakening the cement mantle. Pitto et al.17 described a bone-vacuum technique to limit fat embolism during cemented hip arthroplasty. Three techniques were compared: uncemented, conventional cemented, and bone-vacuum cemented arthroplasties. No embolic events occurred in the uncemented group. Hypotension, arterial oxygen desaturation, and increased pulmonary shunting were significant in the conventional technique, but no changes occurred in these parameters in the uncemented and bone-vacuum techniques. It is most prudent to avoid cementing in patients who cannot tolerate a significant increase in pulmonary shunting. If cementing is required due to poor bone stock, meticulous care should be taken to irrigate and aspirate the intramedullary canal before cement insertion. Recently, there has been a move towards using more uncemented short and long stem components in patients with low pulmonary reserve as adverse cardiopulmonary events have not been reported with these implants.
123
Management of the high-risk patient for either elective or trauma surgery mandates good communication and planning between the orthopedic surgeon and anesthesiologist. As previously stated, fat embolism syndrome, although more common in trauma than in elective procedures, has become a relatively rare occurrence. A recent review from Taiwan reported an incidence of 2.4% in patients with multiple fractures and less than 1% in patients with only a single fracture.18 The current safety of these treatments in both elective and trauma cases is due, in large part, to basic bench research by clinician scientists such as Robert Byrick, and reported here in the Journal. Funding sources
None.
Conflicts of interest
None declared.
References 1. Mellor A, Soni N. Fat embolism. Anaesthesia 2001; 56: 145-54. 2. Johnson MJ, Lucas GL. Fat embolism syndrome. Orthopedics 1996; 19: 41-8. 3. Nixon JR, Brock-Utne JG. Free fatty acid and arterial oxygen changes following major injury: a correlation between hypoxemia and increased free fatty acid levels. J Trauma 1978; 18: 23-6. 4. Akhtar S. Fat embolism. Anesthesiol Clin 2009; 27: 533-50. 5. Blankstein M, Byrick RJ, Nakane M, et al. A preliminary study of platelet activation after embolization of marrow contents. J Orthop Trauma 2012; 26: e214-20. 6. Sulek CA, Davies LK, Enneking FK, Gearen PA, Lobato EB. Cerebral microembolism diagnosed by transcranial Doppler during total knee arthroplasty: correlation with transesophageal echocardiography. Anesthesiology 1999; 91: 672-6. 7. Byrick RJ, Kay JC, Mazer CD, Wang Z, Mullen JB. Dynamic characteristics of cerebral lipid microemboli: videomicroscopy studies in rats. Anesth Analg 2003; 97: 1789-94. 8. Riska EB, Myllynen P. Fat embolism in patients with multiple injuries. J Trauma 1982; 22: 891-4. 9. Eriksson EA, Pellegrini DC, Vanderkolk WE, Minshall CT, Fakhry SM, Cohle SD. Incidence of pulmonary fat embolism at autopsy: an undiagnosed epidemic. J Trauma 2011; 71: 312-5. 10. Christie J, Robinson CM, Pell AC, McBirnie J, Burnett R. Transcardiac echocardiography during invasive intramedullary procedures. J Bone Joint Surg Br 1995; 77: 450-5. 11. Issack PS, Lauerman MH, Helfet DL, Sculco TP, Lane JM. Fat embolism and respiratory distress associated with cemented femoral arthroplasty. Am J Orthop (Belle Mead NJ) 2009; 38: 72-6. 12. Byrick RJ, Forbes D, Waddell JP. A monitored cardiovascular collapse during cemented total knee replacement. Anesthesiology 1986; 65: 213-6. 13. Patterson BM, Healey JH, Cornell CN, Sharrock NE. Cardiac arrest during hip arthroplasty with a cemented long-stem component. A report of seven cases. J Bone Joint Surg Am 1991; 73: 271-7. 14. Byrick RJ, Kay JC, Mullen JB. Pulmonary marrow embolism: a dog model simulating dual component cemented arthroplasty. Can J Anaesth 1987; 34: 336-42. 15. Sherman RM, Byrick RJ, Kay JC, Sullivan TR, Waddell JP. The role of lavage in preventing hemodynamic and blood-gas changes during cemented arthroplasty. J Bone Joint Surg Am 1983; 65: 500-6.
Key article from the journal archives 16. Orsini EC, Byrick RJ, Mullen BM, Kay JC, Waddell JP. Cardiopulmonary function and pulmonary microemboli during arthroplasty using cemented or non-cemented components. The role of intramedullary pressure. J Bone Joint Surg Am 1987; 69: 822-32. 17. Pitto RP, Koessler M, Kuehle JW. Comparison of fixation of the femoral component without cement and fixation with use of a bone-
vacuum cementing technique for the prevention of fat embolism during total hip arthroplasty. A prospective, randomized clinical trial. J Bone Joint Surg Am 1999; 81: 831-43. 18. Tsai IT, Hsu CJ, Chen YH, Fong YC, Hsu HC, Tsai CH. Fat embolism syndrome in long bone fracture—clinical experience in a tertiary referral center in Taiwan. J Chin Med Assoc 2010; 73: 407-10.
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