- Email: [email protected]
Counterpoint: Should Coagulopathy Be Repaired Prior to Central Venous Line Insertion? No
9. 10.
11. 12.
13.
14.
BET 3: central line insertion in deranged clotting. Emerg Med J. 2011;28(6):536-537. Kusminsky RE. Complications of central venous catheterization. J Am Coll Surg. 2007;204(4):681-696. Hébert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl J Med. 1999;340(6):409-417. Goodnough LT. Risks of blood transfusion. Anesthesiol Clin North America. 2005;23(2):241-252. Fiebig EW, Busch MP. Infectious risks of transfusion. In: Spiess BD, Spence RK, Shander A, eds. Perioperative Transfusion Medicine. Philadelphia, PA: Lippincott, Williams and Wilkins; 2006:131-152. Stainsby D. ABO incompatible transfusions-experience from the UK Serious Hazards of Transfusion (SHOT) scheme Transfusions ABO incompatible. Transfus Clin Biol. 2005;1(2): 385-388. Toy P, Lowell C. TRALI—definition, mechanisms, incidence and clinical relevance. Best Pract Res Clin Anaesthesiol. 2007; 21(2):183-193.
Counterpoint: Should Coagulopathy Be Repaired Prior to Central Venous Line Insertion? No concept of “repairing a coagulopathy” is a comTheforting illusion. No one looks forward to insert-
ing a central venous line in a frail patient with an activated partial thromboplastin time greater than assay or an international normalized ratio (INR) of 10 or 12. Our “gut reaction” is to “fix” any abnormal laboratory value prior to placing a central venous line. Therefore, at first glance, the “con” position is counterintuitive and goes against the grain of many established cultural practices and reflexive responses in the hospital setting. These traditions have evolved with the good intention of following two wise mottos: (1) “safety first,” and (2) “primum non nocere.” Nevertheless, upon closer inspection, it turns out that the “cure” of a laboratory-diagnosed coagulopathy is usually elusive. The coagulopathy is usually a manifestation of the underlying disease that required hospitalization. The attempt to “repair” a laboratorydiagnosed coagulopathy can do more harm than the laboratory abnormality itself. That is why I am taking the “con” position in this debate, even though I anticipate that explaining my position will require swimming against the tide. For the purpose of this Point/Counterpoint Editorial, I am assuming that we are defining coagulopathies as abnormal laboratory tests that point to susceptibility to bleeding (eg, prolongation in the prothrombin time or partial thromboplastin time), not clotting. And I am taking an additional leap of faith by presuming that we are discussing primarily 1142
clinically ill patients who are hospitalized, not outpatients who are clinically stable. Among patients who require central venous lines, the surest route to managing the coagulopathy is to fix the underlying problem that is causing the laboratory abnormality. If the patient’s volume status is uncertain, the first step might be to measure the right atrial pressure with a central venous line, especially when clinical assessment (eg, neck surgery) is not feasible. The right atrial pressure measurement will help determine volume status and might help the physician decide whether to administer diuretics (in the presence of a high right atrial pressure) or whether to hydrate in the presence of a low right atrial pressure. Insertion of a central venous line to administer critical drugs through the catheter may be life saving. For example, coagulopathic patients who have septic shock require rapid treatment with multiple antibiotics through a central venous line. Other patients might be hypotensive and critically ill because of cardiogenic shock. They require prompt therapy with potent vasopressors, such as epinephrine, norepinephrine, phenylephrine, dopamine, or dobutamine, administered centrally. Another group of hypotensive patients in shock to consider are those with volume loss, who require rapid rehydration. In all three types of shock, delay in central venous line insertion could be deadly. In the hospital setting, ordering clotting factors or other medications to reverse a laboratory-diagnosed coagulation abnormality is time consuming (Fig 1). Consider the delay in communicating the order to the blood bank or pharmacy, filling the order, transporting the reversal agent to the patient’s bedside, administering the agent, and rechecking the coagulation parameter to determine whether, in fact, it has been normalized. Think of the possible roadblocks
Figure 1. The endless spiral of delay when attempting to “repair” a coagulopathy. Point/Counterpoint Editorials
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on May 3, 2012 © 2012 American College of Chest Physicians
lurking along the way. For example, if an expensive “reversal agent” is ordered, such as recombinant activated factor VII, a mandatory formal “hematology consultation” might be required prior to approving release from the blood bank or pharmacy. The challenges related to urgent central venous line placement in patients with abnormal coagulation values always seem to occur at awkward hours, often in the middle of the night or on major holidays. Sometimes it is difficult to find some of the less commonly used reversal agents. Even transporting the requested agent may not be done properly. For example, have you ever seen fresh frozen plasma, which requires defrosting prior to administration, transported in an ice cooler? Of course, reversal agents are not panaceas. Patients might suffer serious adverse drug reactions, such as anaphylaxis (Table 1). Some of the side effects can be fatal. Of special concern is “rebound thrombosis.” This can occur when the laboratory-diagnosed coagulation abnormality is “normalized” with a reversal agent. In response to this “correction,” the patient might suffer an acute myocardial infarction or stroke. Thus, paradoxically, a critically ill patient who receives a reversal agent to “correct” a laboratory-diagnosed coagulopathy could be worse off clinically, even while appearing “better” on the computer screen displaying the “repaired” coagulation laboratory test results. Furthermore, addressing the medical problems caused by adverse drug reactions to reversal agents must take into account the added expenses of purchasing, storing, and administering these agents. If an abnormal laboratory value is considered so critical as to warrant delaying insertion of a central venous line, then certainly that laboratory value should be rechecked after infusion of the reversal agent. But how soon after administration? And is “normalization” of the abnormal laboratory value going to be the specified criterion prior to central venous line placement? If so, in the presence of a persistently abnormal (albeit improved) laboratorydiagnosed coagulation abnormality, will the process of ordering a reversal agent repeat itself ad infinitum (Fig 1)? We cardiologists deal daily with patients who have an apparent laboratory-diagnosed coagulopathy but Table 1—Adverse Effects of Reversal Agents Reversal Agent
Potential Adverse Effect
IV vitamin K Fresh frozen plasma Recombinant factor VIIa Protamine Prothrombin complex concentrates
www.chestpubs.org
Anaphylaxis Rebound thrombosis, pulmonary edema Rebound thrombosis Anaphylaxis, pulmonary edema Rebound thrombosis
who simultaneously require urgent or emergent cardiac catheterization to manage acute coronary syndrome (ie, unstable angina, non-ST-segment-elevation myocardial infarction, or ST-segment-elevation myocardial infarction). In these situations, we are mostly inserting central arterial lines rather than central venous lines. Our cardiac patients usually take aspirin for primary or secondary prevention of coronary artery disease. Some receive dual antiplatelet therapy, such as aspirin plus clopidogrel, because of prior episodes of acute coronary syndrome or because of prior placement of a drug-eluting coronary artery stent. Others take warfarin to prevent stroke from atrial fibrillation. Urgent or emergent cardiac catheterization might be necessary for a patient taking the dreaded “triple therapy” of aspirin, clopidogrel (or prasugrel or ticagrelor), and warfarin. To make matters worse, the two newer antiplatelet agents, prasugrel1 and ticagrelor,2 cause more bleeding complications than clopidogrel. At the time of the cardiac catheterization, we add heparin or bivalirudin to the patient’s previously established antiplatelet and/or anticoagulant regimen. Have you ever heard of a cardiologist delaying catheterization of a patient with acute myocardial infarction because of an abnormal laboratory parameter indicating a predisposition to bleeding? Of course not. There is no reliable antidote to disaggregated platelets other than “tincture of time.” With clopidogrel, for example, it may take 4 or 5 days before platelet function returns to normal. Thus, in the setting of central venous line insertion during acute myocardial infarction, delay is simply not feasible. From the interventional cardiology perspective, the best way to avoid increased bleeding during insertion of a central line is to practice excellent technique. Experience in the cardiac catheterization laboratory has taught us the hazards of attempting to “repair the coagulopathy.” Patients with acute coronary syndrome are overtly thrombogenic. If we order fresh frozen plasma, for example, we may precipitate an iatrogenic rebound thrombosis. After cessation of IV heparin in patients with acute coronary syndromes, a rebound increase in thrombin generation ensues. Laboratory coagulation parameters that demonstrate this rebound include elevations in fibrinopeptide A and prothrombin fragment 1.2 and a decrease in levels of antithrombin.3 For patients taking longterm warfarin, even a brief interruption may increase the risk of thromboembolism.4 When a central venous line is required, adherence to proper insertion procedures is the key to optimizing patient safety and maximizing the likelihood of successful line placement (Table 2). The major potential complications are pneumothorax, infection, CHEST / 141 / 5 / MAY, 2012
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on May 3, 2012 © 2012 American College of Chest Physicians
1143
Table 2—Technical Pointers for Central Venous Line Insertion 1. Practice with simulations. 2. Become proficient with ultrasonography to identify the vein. 3. Use strict sterile technique. 4. Insist upon a safety pause prior to starting the procedure. 5. Always use ultrasound to guide identification and cannulation of the internal jugular vein.
and inadvertent cannulation of the carotid artery rather than the internal jugular (IJ) vein. Insistence on proper sterile technique is of paramount importance. This begins with ensuring outstanding personal hand hygiene.5 One can counter a laboratory-diagnosed coagulopathy by ensuring that those who insert central lines have extensive training in proper and meticulous technique. At the Mayo Clinic, Internal Medicine house staff undergo a prerotational simulation-based workshop on central venous catheter insertion.6 This educational requirement has improved patient safety. There were 334 procedures in the preeducation period compared with 402 procedures in the posteducation period. The line placement failure rate decreased from 22.8% to 16.2% (P 5 .02), and inadvertent arterial punctures decreased from 4.2% to 1.5% (P 5 .03). Ultrasonography usage increased from 3.0% to 61.4% (P , .01). Instructional videos are an outstanding teaching tool. The best video I have ever seen for ultrasoundguided IJ vein cannulation is an 18-min production of the New England Journal of Medicine.7 Traditionally, when IJ vein cannulation has been performed, external anatomic landmarks and palpation have been used to guide insertion of the needle. Over the past decade, the increased use of ultrasound to guide IJ vein cannulation has improved success rates, reduced the time required to perform the procedure, and resulted in fewer complications. The carotid artery is visualized as a pulsating vessel that does not compress with manual pressure. We must not forget to provide continuous electrocardiographic monitoring and oximetry; we must also be sure to call for a “procedural timeout” and to review a safety checklist prior to getting under way. Passage of the introducer needle into the IJ vein can be performed with either a transverse (short-axis) or a longitudinal (long-axis) view. The transverse view is easier to learn. The longitudinal view allows better visualization of the advancing needle tip, which may reduce perforation of the posterior vessel wall.8 In summary, we must not get sidetracked by abnormal laboratory-diagnosed coagulation parameters in patients who require central venous line placement. We should focus on the indication for the central line and how it might assist in patient management while 1144
maintaining proper sterile technique and using ultrasound guidance for vein cannulation. Samuel Z. Goldhaber, MD, FCCP Boston, MA Affiliations: From the Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School. Financial/nonfinancial disclosures: The author has reported to CHEST the following conflicts of interest: Dr Goldhaber serves as a consultant for the following companies: Baxter, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi Sankyo, Eisai, Medscape, Merck, Portola, and Sanofi Aventis. Correspondence to: Samuel Z. Goldhaber, MD, FCCP, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115; e-mail: [email protected] © 2012 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/ site/misc/reprints.xhtml). DOI: 10.1378/chest.11-3235
References 1. Wiviott SD, Braunwald E, McCabe CH, et al; TRITON-TIMI 38 Investigators. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357(20): 2001-2015. 2. Wallentin L, Becker RC, Budaj A, et al. Ticagelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2009;361(11):1045-1057. 3. Granger CB, Miller JM, Bovill EG, et al. Rebound increase in thrombin generation and activity after cessation of intravenous heparin in patients with acute coronary syndromes. Circulation. 1995;91(7):1929-1935. 4. Garcia DA, Regan S, Henault LE, et al. Risk of thromboembolism with short-term interruption of warfarin therapy. Arch Intern Med. 2008;168(1):63-69. 5. Longtin Y, Sax H, Allegranzi B, Schneider F, Pittet D. Videos in clinical medicine. Hand hygiene. N Engl J Med. 2011; 364(13):e24. 6. Sekiguchi H, Tokita JE, Minami T, Eisen LA, Mayo PH, Narasimhan M. A prerotational, simulation-based workshop improves the safety of central venous catheter insertion: results of a successful internal medicine house staff training program. Chest. 2011;140(3):652-658. 7. Ortega R, Song M, Hansen CJ, Barash P. Videos in clinical medicine. Ultrasound-guided internal jugular vein cannulation. N Engl J Med. 2010;362(16):e57. 8. Feller-Kopman D. Ultrasound-guided internal jugular access: a proposed standardized approach and implications for training and practice. Chest. 2007;132(1):302-309.
Rebuttal From Dr Baron Goldhaber is one of my revered teachers, I AsamDrgratifi ed to see that I have learned well from
him the most important points on which we agree: (1) safety first, and (2) do no harm. As any outstanding teacher will transmit to his or her students, enthusiastic debate is the cornerstone of advancement of our medical understanding and ultimately results in better care of our patients. Thus, I respectfully raise the following in response to the excellent points that Dr Goldhaber has made.1 Point/Counterpoint Editorials
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on May 3, 2012 © 2012 American College of Chest Physicians
11. 12.
13.
14.
BET 3: central line insertion in deranged clotting. Emerg Med J. 2011;28(6):536-537. Kusminsky RE. Complications of central venous catheterization. J Am Coll Surg. 2007;204(4):681-696. Hébert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. N Engl J Med. 1999;340(6):409-417. Goodnough LT. Risks of blood transfusion. Anesthesiol Clin North America. 2005;23(2):241-252. Fiebig EW, Busch MP. Infectious risks of transfusion. In: Spiess BD, Spence RK, Shander A, eds. Perioperative Transfusion Medicine. Philadelphia, PA: Lippincott, Williams and Wilkins; 2006:131-152. Stainsby D. ABO incompatible transfusions-experience from the UK Serious Hazards of Transfusion (SHOT) scheme Transfusions ABO incompatible. Transfus Clin Biol. 2005;1(2): 385-388. Toy P, Lowell C. TRALI—definition, mechanisms, incidence and clinical relevance. Best Pract Res Clin Anaesthesiol. 2007; 21(2):183-193.
Counterpoint: Should Coagulopathy Be Repaired Prior to Central Venous Line Insertion? No concept of “repairing a coagulopathy” is a comTheforting illusion. No one looks forward to insert-
ing a central venous line in a frail patient with an activated partial thromboplastin time greater than assay or an international normalized ratio (INR) of 10 or 12. Our “gut reaction” is to “fix” any abnormal laboratory value prior to placing a central venous line. Therefore, at first glance, the “con” position is counterintuitive and goes against the grain of many established cultural practices and reflexive responses in the hospital setting. These traditions have evolved with the good intention of following two wise mottos: (1) “safety first,” and (2) “primum non nocere.” Nevertheless, upon closer inspection, it turns out that the “cure” of a laboratory-diagnosed coagulopathy is usually elusive. The coagulopathy is usually a manifestation of the underlying disease that required hospitalization. The attempt to “repair” a laboratorydiagnosed coagulopathy can do more harm than the laboratory abnormality itself. That is why I am taking the “con” position in this debate, even though I anticipate that explaining my position will require swimming against the tide. For the purpose of this Point/Counterpoint Editorial, I am assuming that we are defining coagulopathies as abnormal laboratory tests that point to susceptibility to bleeding (eg, prolongation in the prothrombin time or partial thromboplastin time), not clotting. And I am taking an additional leap of faith by presuming that we are discussing primarily 1142
clinically ill patients who are hospitalized, not outpatients who are clinically stable. Among patients who require central venous lines, the surest route to managing the coagulopathy is to fix the underlying problem that is causing the laboratory abnormality. If the patient’s volume status is uncertain, the first step might be to measure the right atrial pressure with a central venous line, especially when clinical assessment (eg, neck surgery) is not feasible. The right atrial pressure measurement will help determine volume status and might help the physician decide whether to administer diuretics (in the presence of a high right atrial pressure) or whether to hydrate in the presence of a low right atrial pressure. Insertion of a central venous line to administer critical drugs through the catheter may be life saving. For example, coagulopathic patients who have septic shock require rapid treatment with multiple antibiotics through a central venous line. Other patients might be hypotensive and critically ill because of cardiogenic shock. They require prompt therapy with potent vasopressors, such as epinephrine, norepinephrine, phenylephrine, dopamine, or dobutamine, administered centrally. Another group of hypotensive patients in shock to consider are those with volume loss, who require rapid rehydration. In all three types of shock, delay in central venous line insertion could be deadly. In the hospital setting, ordering clotting factors or other medications to reverse a laboratory-diagnosed coagulation abnormality is time consuming (Fig 1). Consider the delay in communicating the order to the blood bank or pharmacy, filling the order, transporting the reversal agent to the patient’s bedside, administering the agent, and rechecking the coagulation parameter to determine whether, in fact, it has been normalized. Think of the possible roadblocks
Figure 1. The endless spiral of delay when attempting to “repair” a coagulopathy. Point/Counterpoint Editorials
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on May 3, 2012 © 2012 American College of Chest Physicians
lurking along the way. For example, if an expensive “reversal agent” is ordered, such as recombinant activated factor VII, a mandatory formal “hematology consultation” might be required prior to approving release from the blood bank or pharmacy. The challenges related to urgent central venous line placement in patients with abnormal coagulation values always seem to occur at awkward hours, often in the middle of the night or on major holidays. Sometimes it is difficult to find some of the less commonly used reversal agents. Even transporting the requested agent may not be done properly. For example, have you ever seen fresh frozen plasma, which requires defrosting prior to administration, transported in an ice cooler? Of course, reversal agents are not panaceas. Patients might suffer serious adverse drug reactions, such as anaphylaxis (Table 1). Some of the side effects can be fatal. Of special concern is “rebound thrombosis.” This can occur when the laboratory-diagnosed coagulation abnormality is “normalized” with a reversal agent. In response to this “correction,” the patient might suffer an acute myocardial infarction or stroke. Thus, paradoxically, a critically ill patient who receives a reversal agent to “correct” a laboratory-diagnosed coagulopathy could be worse off clinically, even while appearing “better” on the computer screen displaying the “repaired” coagulation laboratory test results. Furthermore, addressing the medical problems caused by adverse drug reactions to reversal agents must take into account the added expenses of purchasing, storing, and administering these agents. If an abnormal laboratory value is considered so critical as to warrant delaying insertion of a central venous line, then certainly that laboratory value should be rechecked after infusion of the reversal agent. But how soon after administration? And is “normalization” of the abnormal laboratory value going to be the specified criterion prior to central venous line placement? If so, in the presence of a persistently abnormal (albeit improved) laboratorydiagnosed coagulation abnormality, will the process of ordering a reversal agent repeat itself ad infinitum (Fig 1)? We cardiologists deal daily with patients who have an apparent laboratory-diagnosed coagulopathy but Table 1—Adverse Effects of Reversal Agents Reversal Agent
Potential Adverse Effect
IV vitamin K Fresh frozen plasma Recombinant factor VIIa Protamine Prothrombin complex concentrates
www.chestpubs.org
Anaphylaxis Rebound thrombosis, pulmonary edema Rebound thrombosis Anaphylaxis, pulmonary edema Rebound thrombosis
who simultaneously require urgent or emergent cardiac catheterization to manage acute coronary syndrome (ie, unstable angina, non-ST-segment-elevation myocardial infarction, or ST-segment-elevation myocardial infarction). In these situations, we are mostly inserting central arterial lines rather than central venous lines. Our cardiac patients usually take aspirin for primary or secondary prevention of coronary artery disease. Some receive dual antiplatelet therapy, such as aspirin plus clopidogrel, because of prior episodes of acute coronary syndrome or because of prior placement of a drug-eluting coronary artery stent. Others take warfarin to prevent stroke from atrial fibrillation. Urgent or emergent cardiac catheterization might be necessary for a patient taking the dreaded “triple therapy” of aspirin, clopidogrel (or prasugrel or ticagrelor), and warfarin. To make matters worse, the two newer antiplatelet agents, prasugrel1 and ticagrelor,2 cause more bleeding complications than clopidogrel. At the time of the cardiac catheterization, we add heparin or bivalirudin to the patient’s previously established antiplatelet and/or anticoagulant regimen. Have you ever heard of a cardiologist delaying catheterization of a patient with acute myocardial infarction because of an abnormal laboratory parameter indicating a predisposition to bleeding? Of course not. There is no reliable antidote to disaggregated platelets other than “tincture of time.” With clopidogrel, for example, it may take 4 or 5 days before platelet function returns to normal. Thus, in the setting of central venous line insertion during acute myocardial infarction, delay is simply not feasible. From the interventional cardiology perspective, the best way to avoid increased bleeding during insertion of a central line is to practice excellent technique. Experience in the cardiac catheterization laboratory has taught us the hazards of attempting to “repair the coagulopathy.” Patients with acute coronary syndrome are overtly thrombogenic. If we order fresh frozen plasma, for example, we may precipitate an iatrogenic rebound thrombosis. After cessation of IV heparin in patients with acute coronary syndromes, a rebound increase in thrombin generation ensues. Laboratory coagulation parameters that demonstrate this rebound include elevations in fibrinopeptide A and prothrombin fragment 1.2 and a decrease in levels of antithrombin.3 For patients taking longterm warfarin, even a brief interruption may increase the risk of thromboembolism.4 When a central venous line is required, adherence to proper insertion procedures is the key to optimizing patient safety and maximizing the likelihood of successful line placement (Table 2). The major potential complications are pneumothorax, infection, CHEST / 141 / 5 / MAY, 2012
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on May 3, 2012 © 2012 American College of Chest Physicians
1143
Table 2—Technical Pointers for Central Venous Line Insertion 1. Practice with simulations. 2. Become proficient with ultrasonography to identify the vein. 3. Use strict sterile technique. 4. Insist upon a safety pause prior to starting the procedure. 5. Always use ultrasound to guide identification and cannulation of the internal jugular vein.
and inadvertent cannulation of the carotid artery rather than the internal jugular (IJ) vein. Insistence on proper sterile technique is of paramount importance. This begins with ensuring outstanding personal hand hygiene.5 One can counter a laboratory-diagnosed coagulopathy by ensuring that those who insert central lines have extensive training in proper and meticulous technique. At the Mayo Clinic, Internal Medicine house staff undergo a prerotational simulation-based workshop on central venous catheter insertion.6 This educational requirement has improved patient safety. There were 334 procedures in the preeducation period compared with 402 procedures in the posteducation period. The line placement failure rate decreased from 22.8% to 16.2% (P 5 .02), and inadvertent arterial punctures decreased from 4.2% to 1.5% (P 5 .03). Ultrasonography usage increased from 3.0% to 61.4% (P , .01). Instructional videos are an outstanding teaching tool. The best video I have ever seen for ultrasoundguided IJ vein cannulation is an 18-min production of the New England Journal of Medicine.7 Traditionally, when IJ vein cannulation has been performed, external anatomic landmarks and palpation have been used to guide insertion of the needle. Over the past decade, the increased use of ultrasound to guide IJ vein cannulation has improved success rates, reduced the time required to perform the procedure, and resulted in fewer complications. The carotid artery is visualized as a pulsating vessel that does not compress with manual pressure. We must not forget to provide continuous electrocardiographic monitoring and oximetry; we must also be sure to call for a “procedural timeout” and to review a safety checklist prior to getting under way. Passage of the introducer needle into the IJ vein can be performed with either a transverse (short-axis) or a longitudinal (long-axis) view. The transverse view is easier to learn. The longitudinal view allows better visualization of the advancing needle tip, which may reduce perforation of the posterior vessel wall.8 In summary, we must not get sidetracked by abnormal laboratory-diagnosed coagulation parameters in patients who require central venous line placement. We should focus on the indication for the central line and how it might assist in patient management while 1144
maintaining proper sterile technique and using ultrasound guidance for vein cannulation. Samuel Z. Goldhaber, MD, FCCP Boston, MA Affiliations: From the Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School. Financial/nonfinancial disclosures: The author has reported to CHEST the following conflicts of interest: Dr Goldhaber serves as a consultant for the following companies: Baxter, Boehringer Ingelheim, Bristol-Myers Squibb, Daiichi Sankyo, Eisai, Medscape, Merck, Portola, and Sanofi Aventis. Correspondence to: Samuel Z. Goldhaber, MD, FCCP, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115; e-mail: [email protected] © 2012 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/ site/misc/reprints.xhtml). DOI: 10.1378/chest.11-3235
References 1. Wiviott SD, Braunwald E, McCabe CH, et al; TRITON-TIMI 38 Investigators. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357(20): 2001-2015. 2. Wallentin L, Becker RC, Budaj A, et al. Ticagelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2009;361(11):1045-1057. 3. Granger CB, Miller JM, Bovill EG, et al. Rebound increase in thrombin generation and activity after cessation of intravenous heparin in patients with acute coronary syndromes. Circulation. 1995;91(7):1929-1935. 4. Garcia DA, Regan S, Henault LE, et al. Risk of thromboembolism with short-term interruption of warfarin therapy. Arch Intern Med. 2008;168(1):63-69. 5. Longtin Y, Sax H, Allegranzi B, Schneider F, Pittet D. Videos in clinical medicine. Hand hygiene. N Engl J Med. 2011; 364(13):e24. 6. Sekiguchi H, Tokita JE, Minami T, Eisen LA, Mayo PH, Narasimhan M. A prerotational, simulation-based workshop improves the safety of central venous catheter insertion: results of a successful internal medicine house staff training program. Chest. 2011;140(3):652-658. 7. Ortega R, Song M, Hansen CJ, Barash P. Videos in clinical medicine. Ultrasound-guided internal jugular vein cannulation. N Engl J Med. 2010;362(16):e57. 8. Feller-Kopman D. Ultrasound-guided internal jugular access: a proposed standardized approach and implications for training and practice. Chest. 2007;132(1):302-309.
Rebuttal From Dr Baron Goldhaber is one of my revered teachers, I AsamDrgratifi ed to see that I have learned well from
him the most important points on which we agree: (1) safety first, and (2) do no harm. As any outstanding teacher will transmit to his or her students, enthusiastic debate is the cornerstone of advancement of our medical understanding and ultimately results in better care of our patients. Thus, I respectfully raise the following in response to the excellent points that Dr Goldhaber has made.1 Point/Counterpoint Editorials
Downloaded from chestjournal.chestpubs.org by Kimberly Henricks on May 3, 2012 © 2012 American College of Chest Physicians