CASE REPORT
Pressurized Intravenous Fluid Administration in the Professional Football Player: A Unique Setting for Venous Air Embolism Kenton H. Fibel, MD,* Ronnie P. Barnes, ATC,† and James J. Kinderknecht, MD*
Abstract: Venous air embolism (VAE) is a potentially life-threatening event that is most commonly associated with certain surgical procedures, although this theoretical complication of pressurized rapid infusion of intravenous (IV) fluids has been described. This series of cases describes 4 athletes who presented with continuous coughing and other chest complaints after peripheral IV infusion of normal saline through manual pressurized infusion. Symptoms resolved within 20 minutes, and these incidences did not interfere with resuming athletic competition with no recurrence of symptoms or complications. These cases are most consistent with varying degrees of VAE and reveal the risk of VAE associated with pressurized peripheral IV fluid administration along with the unique clinical presentation of more modest forms of VAE in an awake patient. Becoming more knowledgeable about IV infusion technique and understanding potential pitfalls can be helpful in reducing future incidences of VAE. Key Words: venous air embolism, athletes, pressurized intravenous infusion, peripheral IV complications
necessary as symptoms resolved within 20 minutes. These incidences did not interfere with resuming athletic competition with no recurrence of symptoms or complications. Similar infusion sets were used and comprised of a simple latex-free tubing system with a drip chamber size of 15 drops per milliliter and priming volume of 13 mL (IV Administration Set with Universal Spike, Inject Site, and Spin-Lock Connector; B. Braun Medical Inc., Bethlehem, PA). The antecubital fossa was the site of IV access using 18- or 20-G catheters that were 1 inch in length (BD Insyte Autoguard Winged; Beckton Dickinson Infusion Therapy Systems Inc, Sandy, UT). The tubing systems were appropriately flushed before initiating infusion, and the infusions were each pressurized using a manual bulb pump with a steady stream of normal saline that was visualized entering the drip chamber and maintained with episodic bulb pumping. Each player received the entire 1 L volume of a single bag of normal saline (Hospira 0.9% sodium chloride injection; Hospira Inc., Lake Forest, IL) administered over approximately 20 minutes. The bags had not expired and were at room temperature. Players 1, 2, and 3 received their IV infusions for pregame hydration and player 4 for dehydration after practice. The Table outlines the details of each case.
(Clin J Sport Med 2015;25:e67–e69)
INTRODUCTION Venous air embolism (VAE) is a potentially lifethreatening event that is most commonly associated with certain surgical procedures.1 Although VAE has been described as a theoretical complication of pressurized rapid infusion of intravenous (IV) fluids, the documented literature of occurrences is scarce.2 Pressurized infusion is often used to treat severe cramping or pregame hydration in athletes, which may provide a unique setting for increased risk of VAE.
CASE REPORTS Four professional football players presented with similar symptoms and clinical course after peripheral IV infusion of normal saline through manual pressurized infusion during the preseason. Symptoms included continuous coughing with some experiencing chest pain or tightness with deep inspiration. Each player’s vitals, cardiac, and lung examinations were normal. No treatment was Submitted for publication January 29, 2014; accepted July 18, 2014. From the *Department of Medicine, Hospital for Special Surgery, New York, New York; and †New York Giants Medical Services and Training, East Rutherford, New Jersey. The authors report no conflicts of interest. Corresponding Author: Kenton H. Fibel, MD, Hospital for Special Surgery, 535 East 70th St, New York, NY 10021 (fi[email protected]). Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Sport Med Volume 25, Number 4, July 2015
DISCUSSION Potential causes of the athletes’ symptoms initially included pulmonary edema, reactive airway disease, response related to lower relative IV fluid temperature, or latex allergy. However, the clinical presentation was unlikely to be from any of these diagnoses based on the combination of the physical examination, transient symptoms, and presentation directly after IV infusion. After review of the available literature and better understanding of IV fluid administration, each of these cases were felt to represent varying degrees of VAE from pressurized peripheral IV infusion. The true incidence of VAE is unknown and is probably significantly underestimated because of the varying sensitivities of detection methods used during high-risk procedures and unrecognized subclinical VAE.1,3 Additionally, extensive monitoring such as end-tidal carbon dioxide or precordial Doppler ultrasonography is rarely used outside the operating room where other procedures also posing a risk of VAE are commonly performed as with our cases. In this setting, unless sudden cardiorespiratory failure occurs, the clinician must rely on the patient’s subjective complaints or physical examination findings to make the diagnosis of VAE. This requires a high degree of suspicion and familiarity with more modest forms of VAE.1 www.cjsportmed.com |
e67
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Clin J Sport Med Volume 25, Number 4, July 2015
None 20 Sitting None None
31; M
23; M
3
4
None, specifically no history of cardiac or pulmonary issues
18 Sitting then prone None None
18 Sitting None None 28; M 2
| www.cjsportmed.com
M, male; G, gauge; HR, heart rate; BP, blood pressure; wnl, within normal limits; PE, physical examination.
20
None 15
None 20
None 20
Continuous cough HR and BP wnl, no Presented to training and difficulty with abnormal PE room 10 min after deep inspiration findings completion of IV infusion Continuous cough HR and BP wnl, no Presented to training and difficulty with abnormal PE room 15 min after deep inspiration findings completion of IV infusion Cough, right-sided HR and BP wnl, no Began at the time of chest pain abnormal PE completion of IV worsened with findings, infusion deep inspiration symptoms worsened with lying down Continuous cough, HR and BP wnl, no Presented to training retrosternal chest abnormal PE room 10 min after pain and tightness findings completion of IV infusion 18 Sitting Penicillin None
Symptoms Medical History
None, specifically no history of cardiac or pulmonary issues None, specifically no history of cardiac or pulmonary issues None, specifically no history of cardiac or pulmonary issues 25; M
Position While Receiving Gauge Medications Allergies IV Fluids Needle, G Patient Age, yr; No. Sex
TABLE. Clinical Presentations of the Football Players
e68
1
Physical Examination Findings
Initial Time of Presenting Symptoms
Duration of Symptoms, min
Recurrence of Symptoms and Complications
Fibel et al
The clinical presentation of VAE varies significantly depending on the amount of air and the rate that it enters the right ventricle or pulmonary circulation. Although a large volume of air or gas entrainment can lead to complete outflow obstruction of the right ventricle causing heart failure and immediate cardiovascular collapse, more modest amounts of air entrainment into the pulmonary circulation can cause pulmonary vasoconstriction, release of inflammatory mediators, bronchoconstriction, and an increase in ventilation/ perfusion mismatch potentially causing coughing and other symptoms.1 Although only a few cases of VAE in the awake patient are well defined in the literature, they describe complaints of continuous coughing, acute dyspnea, breathlessness, lightheadedness, chest pain,4 and a sense of “impending doom.”1 Attention should be drawn to the commonality that each case presented with the initial symptom of coughing much like our athletes.4–6 Pressurized infusion specifically poses a higher risk of accidental administration of air largely because of its ability to maintain or increase flow by delivering volume at higher pressures to overcome system resistance. System resistance within a simple IV infusion setup is comprised of individual resistors including the catheter, the tubing, the vein, and extravascular tissues surrounding the vein. Higher pressures increase the likelihood of air displacement into the fluid with manual pressure devices particularly requiring much higher peak pressures to produce similar flow compared with constant pressure devices.7,8 This risk is further increased by the substantial amount of air packaged inside the IV bags by the manufacturer, which range anywhere from 50 to 70 mL.2,7,9,10 Better awareness of the safety concerns with pressurized IV fluid infusion can allow for improvement in fluid administration technique and lower the risk of VAE. Suggestions to lower this risk based on the experience of the authors include “double spiking” the IV bag during initial setup by momentarily removing the spike to express packaged air from the bag and then reinserting it. Additionally, infusing the last 100 mL of an IV bag should be avoided as the air–fluid level is closer to the bag outlet, which increases the possibility of air exiting the bag. Utilization of large-volume drip chambers may allow air exiting the bag to escape the fluid before traveling into the tubing.7,10 Other recommendations include decreasing system resistance by using wider bore tubing, catheter size of 18 G or less, and using veins in the proximal forearm or antecubital fossa. It should also be emphasized that unless deemed necessary, rapid infusion should be avoided as this alone can greatly reduce risk of VAE with pressurized infusion. Because implementing these changes into our IV administration protocol, we have had no further incidences. In conclusion, this case series reveals the risk of VAE associated with pressurized peripheral IV fluid administration and the unique clinical presentation of more modest forms of VAE in an awake patient. Becoming more knowledgeable about IV infusion technique and understanding potential pitfalls can be helpful in reducing future incidences of VAE. Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Clin J Sport Med Volume 25, Number 4, July 2015
REFERENCES 1. Mirski MA, Lele AV, Fitzsimmons L, et al. Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007;106:164–177. 2. Philip JH. Intravenous access and delivery principles. In: Rogers MC, Tinker JH, Covino BG, et al., eds. Principles and Practice of Anesthesiology. St. Louis. Mosby Year Book; 1992:1183–1196. 3. Hong JY, Kim WO, Kil HK. Detection of subclinical CO2 embolism by transesophageal echocardiography during laparoscopic radical prostatectomy. Urology. 2010;75:581–584. 4. Suarez S, Ornaque I, Fabregas N, et al. Venous air embolism during Parkinson surgery in patients with spontaneous ventilation. Anesth Analg. 1999;88:793–794. 5. Imai S, Tamada T, Gyoten M, et al. Iatrogenic venous air embolism caused by CT injector—from a risk management point of view. Radiat Med. 2004;22:269–271.
Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
Venous Air Embolism in the Football Player 6. Balki M, Manninen PH, McGuire GP, et al. Venous air embolism during awake craniotomy in a supine patient. Can J Anesthesiol. 2003;50:835– 838. 7. Philip BK, Philip JH. Avoiding air infusion with pressurized infusion systems: a new hazard. Anesth Analg. 1985;64:381–382. 8. Goodie DB. The effect of manual bulb pump infusion systems on venous luminal pressure and vein wall integrity. Anesth Analg. 1995;80:552– 556. 9. Feuerman J, Avula R, Smith CE. IV Fluid Administration: How Much Air Is in Crystalloid and Colloid Bags? Cleveland, OH: Department of Anesthesia, MetroHealth Medical Center, Case Western Reserve University. www.anesthesiawiki.net/metrohealthanesthesia/MHAnes/research/ abstracts/abAirIVBag2004.doc. Accessed September 15, 2013. 10. Adhikary GS, Massey SR. Massive air embolism: a case report. J Clin Anesth. 1998;10:70–72.
www.cjsportmed.com |
e69
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Pressurized Intravenous Fluid Administration in the Professional Football Player: A Unique Setting for Venous Air Embolism Kenton H. Fibel, MD,* Ronnie P. Barnes, ATC,† and James J. Kinderknecht, MD*
Abstract: Venous air embolism (VAE) is a potentially life-threatening event that is most commonly associated with certain surgical procedures, although this theoretical complication of pressurized rapid infusion of intravenous (IV) fluids has been described. This series of cases describes 4 athletes who presented with continuous coughing and other chest complaints after peripheral IV infusion of normal saline through manual pressurized infusion. Symptoms resolved within 20 minutes, and these incidences did not interfere with resuming athletic competition with no recurrence of symptoms or complications. These cases are most consistent with varying degrees of VAE and reveal the risk of VAE associated with pressurized peripheral IV fluid administration along with the unique clinical presentation of more modest forms of VAE in an awake patient. Becoming more knowledgeable about IV infusion technique and understanding potential pitfalls can be helpful in reducing future incidences of VAE. Key Words: venous air embolism, athletes, pressurized intravenous infusion, peripheral IV complications
necessary as symptoms resolved within 20 minutes. These incidences did not interfere with resuming athletic competition with no recurrence of symptoms or complications. Similar infusion sets were used and comprised of a simple latex-free tubing system with a drip chamber size of 15 drops per milliliter and priming volume of 13 mL (IV Administration Set with Universal Spike, Inject Site, and Spin-Lock Connector; B. Braun Medical Inc., Bethlehem, PA). The antecubital fossa was the site of IV access using 18- or 20-G catheters that were 1 inch in length (BD Insyte Autoguard Winged; Beckton Dickinson Infusion Therapy Systems Inc, Sandy, UT). The tubing systems were appropriately flushed before initiating infusion, and the infusions were each pressurized using a manual bulb pump with a steady stream of normal saline that was visualized entering the drip chamber and maintained with episodic bulb pumping. Each player received the entire 1 L volume of a single bag of normal saline (Hospira 0.9% sodium chloride injection; Hospira Inc., Lake Forest, IL) administered over approximately 20 minutes. The bags had not expired and were at room temperature. Players 1, 2, and 3 received their IV infusions for pregame hydration and player 4 for dehydration after practice. The Table outlines the details of each case.
(Clin J Sport Med 2015;25:e67–e69)
INTRODUCTION Venous air embolism (VAE) is a potentially lifethreatening event that is most commonly associated with certain surgical procedures.1 Although VAE has been described as a theoretical complication of pressurized rapid infusion of intravenous (IV) fluids, the documented literature of occurrences is scarce.2 Pressurized infusion is often used to treat severe cramping or pregame hydration in athletes, which may provide a unique setting for increased risk of VAE.
CASE REPORTS Four professional football players presented with similar symptoms and clinical course after peripheral IV infusion of normal saline through manual pressurized infusion during the preseason. Symptoms included continuous coughing with some experiencing chest pain or tightness with deep inspiration. Each player’s vitals, cardiac, and lung examinations were normal. No treatment was Submitted for publication January 29, 2014; accepted July 18, 2014. From the *Department of Medicine, Hospital for Special Surgery, New York, New York; and †New York Giants Medical Services and Training, East Rutherford, New Jersey. The authors report no conflicts of interest. Corresponding Author: Kenton H. Fibel, MD, Hospital for Special Surgery, 535 East 70th St, New York, NY 10021 (fi[email protected]). Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Sport Med Volume 25, Number 4, July 2015
DISCUSSION Potential causes of the athletes’ symptoms initially included pulmonary edema, reactive airway disease, response related to lower relative IV fluid temperature, or latex allergy. However, the clinical presentation was unlikely to be from any of these diagnoses based on the combination of the physical examination, transient symptoms, and presentation directly after IV infusion. After review of the available literature and better understanding of IV fluid administration, each of these cases were felt to represent varying degrees of VAE from pressurized peripheral IV infusion. The true incidence of VAE is unknown and is probably significantly underestimated because of the varying sensitivities of detection methods used during high-risk procedures and unrecognized subclinical VAE.1,3 Additionally, extensive monitoring such as end-tidal carbon dioxide or precordial Doppler ultrasonography is rarely used outside the operating room where other procedures also posing a risk of VAE are commonly performed as with our cases. In this setting, unless sudden cardiorespiratory failure occurs, the clinician must rely on the patient’s subjective complaints or physical examination findings to make the diagnosis of VAE. This requires a high degree of suspicion and familiarity with more modest forms of VAE.1 www.cjsportmed.com |
e67
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Clin J Sport Med Volume 25, Number 4, July 2015
None 20 Sitting None None
31; M
23; M
3
4
None, specifically no history of cardiac or pulmonary issues
18 Sitting then prone None None
18 Sitting None None 28; M 2
| www.cjsportmed.com
M, male; G, gauge; HR, heart rate; BP, blood pressure; wnl, within normal limits; PE, physical examination.
20
None 15
None 20
None 20
Continuous cough HR and BP wnl, no Presented to training and difficulty with abnormal PE room 10 min after deep inspiration findings completion of IV infusion Continuous cough HR and BP wnl, no Presented to training and difficulty with abnormal PE room 15 min after deep inspiration findings completion of IV infusion Cough, right-sided HR and BP wnl, no Began at the time of chest pain abnormal PE completion of IV worsened with findings, infusion deep inspiration symptoms worsened with lying down Continuous cough, HR and BP wnl, no Presented to training retrosternal chest abnormal PE room 10 min after pain and tightness findings completion of IV infusion 18 Sitting Penicillin None
Symptoms Medical History
None, specifically no history of cardiac or pulmonary issues None, specifically no history of cardiac or pulmonary issues None, specifically no history of cardiac or pulmonary issues 25; M
Position While Receiving Gauge Medications Allergies IV Fluids Needle, G Patient Age, yr; No. Sex
TABLE. Clinical Presentations of the Football Players
e68
1
Physical Examination Findings
Initial Time of Presenting Symptoms
Duration of Symptoms, min
Recurrence of Symptoms and Complications
Fibel et al
The clinical presentation of VAE varies significantly depending on the amount of air and the rate that it enters the right ventricle or pulmonary circulation. Although a large volume of air or gas entrainment can lead to complete outflow obstruction of the right ventricle causing heart failure and immediate cardiovascular collapse, more modest amounts of air entrainment into the pulmonary circulation can cause pulmonary vasoconstriction, release of inflammatory mediators, bronchoconstriction, and an increase in ventilation/ perfusion mismatch potentially causing coughing and other symptoms.1 Although only a few cases of VAE in the awake patient are well defined in the literature, they describe complaints of continuous coughing, acute dyspnea, breathlessness, lightheadedness, chest pain,4 and a sense of “impending doom.”1 Attention should be drawn to the commonality that each case presented with the initial symptom of coughing much like our athletes.4–6 Pressurized infusion specifically poses a higher risk of accidental administration of air largely because of its ability to maintain or increase flow by delivering volume at higher pressures to overcome system resistance. System resistance within a simple IV infusion setup is comprised of individual resistors including the catheter, the tubing, the vein, and extravascular tissues surrounding the vein. Higher pressures increase the likelihood of air displacement into the fluid with manual pressure devices particularly requiring much higher peak pressures to produce similar flow compared with constant pressure devices.7,8 This risk is further increased by the substantial amount of air packaged inside the IV bags by the manufacturer, which range anywhere from 50 to 70 mL.2,7,9,10 Better awareness of the safety concerns with pressurized IV fluid infusion can allow for improvement in fluid administration technique and lower the risk of VAE. Suggestions to lower this risk based on the experience of the authors include “double spiking” the IV bag during initial setup by momentarily removing the spike to express packaged air from the bag and then reinserting it. Additionally, infusing the last 100 mL of an IV bag should be avoided as the air–fluid level is closer to the bag outlet, which increases the possibility of air exiting the bag. Utilization of large-volume drip chambers may allow air exiting the bag to escape the fluid before traveling into the tubing.7,10 Other recommendations include decreasing system resistance by using wider bore tubing, catheter size of 18 G or less, and using veins in the proximal forearm or antecubital fossa. It should also be emphasized that unless deemed necessary, rapid infusion should be avoided as this alone can greatly reduce risk of VAE with pressurized infusion. Because implementing these changes into our IV administration protocol, we have had no further incidences. In conclusion, this case series reveals the risk of VAE associated with pressurized peripheral IV fluid administration and the unique clinical presentation of more modest forms of VAE in an awake patient. Becoming more knowledgeable about IV infusion technique and understanding potential pitfalls can be helpful in reducing future incidences of VAE. Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Clin J Sport Med Volume 25, Number 4, July 2015
REFERENCES 1. Mirski MA, Lele AV, Fitzsimmons L, et al. Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007;106:164–177. 2. Philip JH. Intravenous access and delivery principles. In: Rogers MC, Tinker JH, Covino BG, et al., eds. Principles and Practice of Anesthesiology. St. Louis. Mosby Year Book; 1992:1183–1196. 3. Hong JY, Kim WO, Kil HK. Detection of subclinical CO2 embolism by transesophageal echocardiography during laparoscopic radical prostatectomy. Urology. 2010;75:581–584. 4. Suarez S, Ornaque I, Fabregas N, et al. Venous air embolism during Parkinson surgery in patients with spontaneous ventilation. Anesth Analg. 1999;88:793–794. 5. Imai S, Tamada T, Gyoten M, et al. Iatrogenic venous air embolism caused by CT injector—from a risk management point of view. Radiat Med. 2004;22:269–271.
Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
Venous Air Embolism in the Football Player 6. Balki M, Manninen PH, McGuire GP, et al. Venous air embolism during awake craniotomy in a supine patient. Can J Anesthesiol. 2003;50:835– 838. 7. Philip BK, Philip JH. Avoiding air infusion with pressurized infusion systems: a new hazard. Anesth Analg. 1985;64:381–382. 8. Goodie DB. The effect of manual bulb pump infusion systems on venous luminal pressure and vein wall integrity. Anesth Analg. 1995;80:552– 556. 9. Feuerman J, Avula R, Smith CE. IV Fluid Administration: How Much Air Is in Crystalloid and Colloid Bags? Cleveland, OH: Department of Anesthesia, MetroHealth Medical Center, Case Western Reserve University. www.anesthesiawiki.net/metrohealthanesthesia/MHAnes/research/ abstracts/abAirIVBag2004.doc. Accessed September 15, 2013. 10. Adhikary GS, Massey SR. Massive air embolism: a case report. J Clin Anesth. 1998;10:70–72.
www.cjsportmed.com |
e69
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
