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Cardiac tamponade after removal of atrial intracardiac monitoring catheters in a pediatric patient: Case report
Cardiac tamponade after removal of atrial intracardiac monitoring catheters in a pediatric patient: Case report Linda J. Johnston, RN, BSc, PhD,a,b and D.F. McKinley, RN, BAppSci, MN,b Melbourne, Australia
The incidence of cardiac tamponade after cardiac surgery is reported as ranging from 0.04% to 7%. Although a relatively infrequent complication, tamponade is associated with significant morbidity and mortality. Reports of tamponade after pediatric cardiac surgery are few and generally associated with postcardiotomy syndrome or, less commonly, removal of left atrial or pulmonary artery catheters after surgery. A case is presented of cardiac tamponade in a pediatric patient resulting from removal of a direct atrial and a pulmonary artery catheter after cardiac surgery. The pathophysiology of cardiac tamponade is reviewed and the increased risk for pediatric patients is outlined. The case review is conducted in the context of existing policies in the reporting institution and recommendations for practice are discussed. (Heart Lung® 2000;29:256-61.)
A
cute cardiac tamponade is a rare but lifethreatening complication after cardiac surgery. Tamponade after cardiac surgery may be an early complication in the initial 7-day postoperative period. It may also be a late complication, occurring up to 6 months after surgery.1-3 The time of occurrence may be related to the etiology. Coagulopathies that occur in association with cardiopulmonary bypass combined with inadequate surgical hemostasis are the usual cause of early cardiac tamponade. Although the aortic suture line and atriotomy are common bleeding sites, discrete sites may not necessarily be identified. Early tamponade may also occur as a complication of removal of intracardiac monitoring catheters. In a 10-year review of 6690 intracardiac monitoring catheters in 5666 pediatric patients From the aVictorian Centre for Nursing Practice Research and bRoyal Children’s Hospital. Reprint requests: Linda J. Johnston, RN, BSc, PhD, Senior Research Fellow, The Victorian Centre for Nursing Practice Research, University of Melbourne, Level 1, 723 Swanston St, Carlton, Victoria, 3053 Australia. Copyright © 2000 by Mosby, Inc. 0147-9563/2000/$12.00 + 0 2/1/106208 doi:10.1067/mhl.2000.106208
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undergoing cardiac surgical procedures, an overall bleeding complication rate of 0.22% was identified. Of these patients, 0.04% had an associated tamponade.4 Tamponade has also been described in adults secondary to the removal of epicardial pacing wires.5,6 Although most reports of late tamponade have been described in adults, it has also been described in children after aortopulmonary anastomoses2,7 and occasionally after atrial septal defect repairs and insertion of intra-atrial baffles.2 Late tamponade may occur as a result of postcardiotomy syndrome and anticoagulation therapy.1,2,8 As a complication of postcardiotomy syndrome tamponade is infrequent, yet it is reported more in the pediatric age group than in adults.9 In neonates, tamponade is also a recognized iatrogenic complication of central venous line placement, administration of fluids, or both.10-15
PATHOPHYSIOLOGY The pericardial sac surrounding the heart is composed of fibrous tissue with little elasticity. The sac contains a small volume of fluid that serves to cushion and protect the myocardium.16 The inextensibility of the pericardium means the heart
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Cardiac tamponade after removal of atrial catheters
Fig 1 Major hemodynamic changes and compensatory mechanisms associated with cardiac tamponade. As cardiac output decreases, compensatory mechanisms driven by the sympathetic nervous system are activated. Although the initial response will result in an increase in cardiac output, unalleviated tamponade will eventually overwhelm the compensatory mechanisms. The increase in heart rate increases myocardial oxygen requirements and shortens ventricular filling time leading to an additional decrease in stroke volume and coronary perfusion. Peripheral vasoconstriction may increase afterload to the point that ventricular ejection is compromised. Closed arrows, Succession of events in tamponade; open arrows, compensatory mechanisms.
and pericardial contents compete continuously for a relatively fixed intrapericardial volume. As such, a slow accumulation of fluid may be accommodated by a progressively stretching pericardium. In contrast, rapid accumulation of fluid in the relatively noncompliant surrounds of the pericardium will be at the expense of cardiac chamber volume.3,17-19 If unchecked by the major compensatory mechanisms, the continued compression of the ventricular and atrial volumes will lead to resistance to car-
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diac filling and a progressive reduction in ventricular stroke volume (Fig 1). Classically, tamponade is defined by a group of symptoms known as Beck’s triad: the heart is small and heart sounds are muffled, the venous pressure is elevated, and the systemic arterial pressure is decreased.20 Tamponade is clinically apparent as tachycardia, a narrowed pulse pressure, peripheral vasoconstriction evidenced by clammy, cold extremities and reduced perfusion, and, eventual-
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ly, hypotension.21 Dyspnea, abdominal symptoms, and the sinus tachycardia are the more common symptoms associated with tamponade.22 The condition may also be indicated by pulsus paradoxus. Normally, as intrathoracic pressure decreases during inspiration, right atrial pressure decreases and venous return to the right heart is augmented. Concurrently, the pulmonary vasculature expands, leading to increased venous pooling in the lungs and a subsequent reduction in left ventricular filling, resulting in a decreased stroke volume and a fall in systolic pressure of less than 10 mm Hg.21 The inspiratory decline in systolic pressure is excessive (ie, greater than 10 mm Hg), as the increase in right heart volume because of tamponade increases the intrapericardial pressure even further and transmural (intrapericardial versus intrapleural) pressure falls. This phenomenon of respiratory reciprocation where inspiration increases right heart filling at the expense of left heart filling with reversal on expiration is expressed as pulsus paradoxus.19,20,23 In the patient with positive pressure ventilation, pulsus paradoxus may in fact be reversed.1,24 Positive pulsus paradoxus is identified by an exaggerated rise (>10 mm Hg) in systolic pressure during inspiration.25 It may also be absent in tamponade associated with left ventricular failure, hypovolemia, atrial septal defect, or severe aortic incompetence.21 Pulsus paradoxus may be determined in those patients with an indwelling arterial catheter by observing the decline in systolic blood pressure during the inspiratory cycle. Pulse oximetry may be a noninvasive method for measuring the degree of pulsus paradoxus in the pediatric patient who is not receiving ventilation.26 This measurement, which is technically more challenging to get, is obtained through measuring the respiratorydependent changes of the pulse waveform on the oximeter.
Altered hemostasis in children after cardiac surgery The anticipated response for every patient whose blood has been subjected to the nonendothelialized bypass circuit is a predisposition to clot formation and platelet activation. As such, patients are routinely heparinized during bypass, resulting in an increased risk of excessive bleeding after surgery as a result of the associated disturbed platelet function and fibrinolysis.27,28 In neonates and infants, altered hemostasis is exacerbated by the hemodilution effect resulting from a relatively large circuit prime to small blood volume ratio and
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the severe inflammatory response and release of associated mediators that is magnified by deep hypothermia and circulatory arrest. In addition, there are altered responses to heparinization. These include delayed hepatic clearance and the reduction in the effectiveness of clotting factors as a result of the hemodilution.29 Pediatric patients undergoing cardiac surgery are subject to additional disturbances in hemostasis after cardiopulmonary bypass because of factors related to their being children with congenital heart disease. Altered hepatic function in association with congenital heart disease can occur through low cardiac output, hemodynamic instability, or rarely, inferior vena caval obstruction. Also, in infants up to 6 months of age, immature hepatic synthetic function prolongs the activated partial thromboplastin time.30,31 This immature function is related to decreased levels of contact factors (eg, factor XII, XI, prekallikrein, and high molecular weight kininogen).32 Bleeding is also potentially worse in the presence of cyanotic congenital heart disease because of associated thrombocytopenia and platelet dysfunction.29 Other relevant associations are the use of prostaglandin E, asplenia, technical surgical complexity involving extensive reconstruction and suturing, reoperation through vascular scar, and the resultant prolonged bypass time.32
Monitoring in the pediatric patient after cardiac surgery Invasive hemodynamic monitoring is an essential component of postoperative assessment after pediatric cardiac surgery. One component of this assessment, and one that is common to the pediatric population, is the measurement of pressures via direct transthoracic, intracardiac monitoring catheters. These 19-gauge catheters are easily placed in the heart under direct vision at the time of surgery, secured with a purse-string suture to the epicardium, and exit the mediastinum via the chest wall. Thus unlike in monitoring in the adult patient, pulmonary artery catheters are not routinely used.33,34 The patency of these catheters after surgery is maintained with a heparinized continuous infusion. Right atrial pressure provides a measurement of systemic venous return, vascular volume, and function of right side of the heart. Monitoring of left atrial pressure provides information about pulmonary venous pressure, left ventricular preload and function, and systemic volume. Measurement of pulmonary artery pressure is an indicator of right ventricular function and outflow tract patency, pulmonary vascular reactivity, venous pressure in the
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Table Clotting profile of the patient before removal of direct transthoracic monitoring catheters* Patient (RCH Reference Range)
Fibrinogen (g/L) Platelets (×109/L) PT (s) PTT (s)
4.6 59 16.2 37
(1.5-4) (150-400) (12-16) (27-38)
Accepted in ICU patient
183 161 13.9 63.7
± ± ± ±
33 (% activity) 65 1.7 14.1
PT, Prothrombin time; PTT, partial thromboplastin time. *The Royal Children’s Hospital (RCH) Reference Range and those identified as acceptable in the ICU patient 24 hours after surgery are shown for comparison.32
lungs, and mean filling pressure on the left side of the heart.34,35 Direct intracardiac catheters are generally reserved for hemodynamic monitoring and are removed after the acute postoperative period.
CASE REPORT Baby P was born at term (birth weight, 3.3 kg) by normal vaginal delivery to a gravida 9, para 7 mother. Antenatal ultrasonagraphy suggested a cardiac abnormality and possible Down syndrome. Postnatal chromosome analysis and echocardiography confirmed the genetic diagnosis and revealed a complete atrioventricular septal defect with a small patent ductus arteriosus. With severe failure to thrive and hospitalized since birth, she was transferred to our institution at the age of 6 weeks for surgical intervention and continuation of care. A complete repair was undertaken with a degree of left and right atrioventricular (AV) valve incompetence evident at time of surgery. Pulmonary hypertension and continued ventilator dependence after surgery necessitated additional surgery 13 days later for poor left AV valve function. Both right and left AV valves were revised with some improvement in function. Cardiopulmonary bypass time was 71 minutes, and the patient’s temperature was lowered to 28°C. Pacing wires, a left atrial (LA) catheter, pulmonary artery catheter, Tenckhoff peritoneal catheter, and 2 mediastinal chest drains were inserted per routine, and the patient was transferred to the intensive care unit. The initial course after surgery was unremarkable, and both chest drains were removed on day 2 after minimal drainage in total and no drainage over the preceding 12 hours. On the fourth day after surgery the direct monitoring catheters were removed. Six hours before removal of the catheters
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the associated heparinized infusions were discontinued. A clotting profile revealed a low platelet count, a normal activated partial prothrombin time, prolonged prothrombin time, and an elevated fibrinogen level (Table). Subsequently, 37 mL (10 mL/kg) of platelets was administered 1 hour before removal of the LA catheter. Blood loss from the site after removal was estimated at 15 mL and was associated with a decrease in mean arterial pressure (MAP) from 68 to 40 mm Hg. The administration of 20 mL of 4% albumin resulted in a significant improvement in the MAP to 50 mm Hg. Fifteen minutes later, in consultation with medical staff, the pulmonary artery catheter was removed. Continuous ooze was accompanied by a marked deterioration in the patient’s color, a decrease in MAP to 25 mm Hg, bradycardia, and loss of a pulsatile arterial trace on the monitor. Immediate resuscitation consisted of cardiac compressions, adrenaline, volume expansion, hand ventilation, and needle aspiration of 8 mL bloody fluid from the pericardial space. Subsequently, cardiac tamponade was diagnosed by echocardiography. The sternotomy wound was opened with the patient under general anesthetic in the ICU, and the pericardial space was entered. Approximately 200 mL of blood and clots were removed from the pericardial cavity. Continuous bleeding from the heart muscle was noted at the site of the LA catheter removal and was oversewn with achievement of hemostasis. Physicians completed a standard sternotomy closure and inserted a single chest drain; the infant was in a stable condition. A stormy course after surgery complicated by an inability to wean from the ventilator necessitated plication of the diaphragm and additional mitral and tricuspid valve repair. The infant was trans-
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ferred back to the referring hospital at 31⁄2 months of age with oxygen saturations above 90% in room air (FiO2 0.21); in addition, the infant received diuretics, an angiotensin-converting enzyme inhibitor, sodium supplements, and breastfeeding, but required nasogastric tube feeding supplements.
DISCUSSION Management of the pediatric patient after cardiac surgery varies between institutions. At our institution, hemodynamic monitoring catheters are routinely removed 4 days after surgery when the patient has usually been transferred to the cardiac surgery unit for continued care. Once the decision has been made to stop monitoring, those lines that have had continuous heparinized infusions remain in situ and are turned off for 24 hours before removal. Unit policy dictates that lines are removed (1) during the day when surgeons are available, (2) when the blood coagulation profile is normal (platelets may be administered before removal if indicated), and (3) only with the written order of the surgeon. The technique for removal is one of even, gentle traction followed by continued pressure over the insertion site for a couple of minutes. Any oozing from the site is noted and the dressing reinforced. As the direct atrial lines are sutured into cardiac muscle, the patient is observed closely for signs of bleeding, effusion, or cardiac tamponade. The onset of pallor, tachypnea, and tachycardia are particularly noted. If the child is still in the ICU, heart rate, oxygen saturation, and blood pressure will be continuously monitored. However, in most instances the child will have been transferred to the cardiac surgery unit without continuous monitoring, and an echocardiograph is obtained within hours of catheter removal. Although the use of direct transthoracic monitoring catheters is not a simple undertaking, neither is their removal. Entrapment, bleeding, and tamponade may be associated complications. Death may even result. The removal of direct monitoring catheters on the first or second day after surgery and before removal of chest drains may enable drainage and the detection of such bleeding.4 However, consideration should also be given to the altered hematologic status that may be present in these patients at this relatively early point in the postoperative recovery period as a result of undergoing cardiopulmonary bypass. In the reporting institution, the chest drain is removed when drainage is considered minimal, usually the day
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after surgery. Direct monitoring catheters remain in situ until day 4 after surgery to minimize the risk of bleeding that may be associated with removal. Before removal of direct transthoracic monitoring catheters, it is recommended that crossmatched blood and platelets be available and that patients be checked for coagulopathies and abnormalities corrected. Administration of platelets will normally rectify a coagulopathy, and it is not routine to recheck the platelet count after transfusion. An infusion of 70 mL platelets per 5 kg body weight should increase the count by 50 × 109/L.36 When more than 1 line is being removed simultaneously, as in the case study described, active bleeding at the first site should be treated with a high index of suspicion and the platelet count rechecked. In the case presented, re-exploration of the sternotomy identified the origin of the bleeding as the previous site of the LA catheter, the first catheter to be removed. Compensatory mechanisms in the pediatric patient will maintain the blood pressure initially. Tachycardia and vasoconstriction with cool and mottled extremities will be apparent. It is not until blood loss reaches 30 mL/kg, almost half the total blood volume, that blood pressure will fall.37 In the event of continued bleeding despite previous supposed correction of a coagulopathy, additional blood products and surgical exploration will be required. The nurse caring for the pediatric patient after cardiac surgery must be aware of the signs of impending tamponade. Close observation will identify the tachycardia and pallor associated with an acute and large volume of blood loss before a terminal bradycardia and hypotension eventuate. Identification of the child with a slower accumulation of blood in the pericardial space may be more difficult. Recognition of an increasing hypoxia, sometimes manifested as disorientation or unusual behavior, may be confounded by other factors, such as the developmental age of the child and the psychologic response to hospitalization and the surgery. Clinical decision making should always be based on sound knowledge and informed by current institution policy. Heightened awareness of this rarely seen clinical condition may be promoted by regular education sessions and attendance by nursing staff at scheduled morbidity and mortality meetings. In conclusion, although tamponade in the pediatric patient after cardiac surgery may be a rare occurrence, the nurse caring for these patients should be vigilant in the assessment of this “at-
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risk” patient population and recognition of this complication.
REFERENCES 1. Keck S, Anderson C, Rieth J. Cardiac tamponade: an initial study in the development of a predictive tool. Heart Lung 1983;12(5):505-9. 2. Kron I, Rheuban K, Nolan S. Late cardiac tamponade in children. Ann Surg 1984;199(2):173-5. 3. Zator Estes M. Management of the cardiac tamponade patient: a nursing framework. Crit Care Nurse 1985;5(5): 17-26. 4. Gold J, Jonas R, Lang P, Elixson E, Mayer J, Castaneda A. Transthoracic intracardiac monitoring lines in pediatric surgical patients: a 10-year experience. Ann Thorac Surg 1986; 42:185-91. 5. Baldwin B, Dorney E. Acute cardiac tamponade following the removal of temporary epicardial pacemaker wires after open heart surgery. Am J Med Sci 1971;261(5):241-3. 6. Hoidal C. Pericardial tamponade after removal of a epicardial pacemaker wire. Crit Care Med 1986;14(4):305-6. 7. Radley-Smith R, Gonzales-Lavin L, Somerville J. Pericardial effusion with tamponade following anastomosis of the ascending aorta to the right pulmonary artery. J Thorac Cardiovasc Surg 1970;60:565-74. 8. Belic L, Stafford G, Allen J, Venkataraman K. Cardiac tamponade during anticoagulation. JAMA 1978;240(7):672. 9. Ofori-Krakye SK, Tyberg TI, Geha AS, Hammond GL, Cohen LS, Langou RA. Late cardiac tamponade after open heart surgery: incidence, role of anticoagulants in its pathogenesis, and its relationship to the postpericardiotomy syndrome. Circulation 1981;63(6):1323-8. 10. Opitz JC, Toyama W. Cardiac tamponade from central venous catheterization: two cases in premature infants with survival. Pediatrics 1982;70(1):139-40. 11. Agarwal KC, Khan MA, Falla A, Amato JJ. Cardiac perforation from central venous catheters: survival after cardiac tamponade in an infant. Pediatrics 1984;73(3):333-8. 12. Rogers BB, Berns SD, Maynard EC, Hansen TW. Pericardial tamponade secondary to central venous catheterization and hyperalimentation in a very low birth weight infant. Pediatric Pathol 1990;10(5):819-23. 13. Mupanemunda RH, Mackanjee HR. A life-threatening complication of percutaneous central venous catheters in neonates. Am J Dis Child 1992;146(12):1414-5. 14. Wirrell EC, Pelausa EO, Allen AC, Stinson DA, Hanna BD. Massive pericardial effusion as a cause for sudden deterioration of a very low birth weight infant. Am J Perinatol 1993;10(6): 419-23. 15. Fioravanti J, Buzzard C, Harris J. Pericardial effusion and tamponade as a result of percutaneous Silastic catheter use. Neonat Netw 1998;17(5):39-42. 16. Gabella G. Cardiovascular. Gray’s anatomy. 38th ed. New York: Churchill Livingstone; 1995. p. 1451-626. 17. Reddy P, Curtiss E, O’Toole J, Shaver J. Cardiac tamponade: hemodynamic observations in man. Circulation 1978;58(2): 265-72.
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Cardiac tamponade after removal of atrial catheters 18. Reddy P, Curtiss E, Uretsky B. Spectrum of hemodynamic changes in cardiac tamponade. Am J Cardiol 1990;66:1487-91. 19. Spodick D. Pathophysiology of cardiac tamponade. Chest 1998;113:1372-8. 20. Kirklin J, Barratt-Boyes B. Cardiac surgery. 2nd ed. New York: John Wiley and Sons; 1993. 21. Hoffman J, Stanger P. Diseases of the pericardium. In: Rudolph A, Hoffman J, Rudolph C, editors. Rudolph’s pediatrics. 20th ed. Stamford (CT): Appleton and Lang; 1996. p. 1530-1. 22. Scarpinato L. Perciardial effusion and cardiac tamponade diagnositic methods: where are we headed? Chest 1996;110(2):308-10. 23. Shabetai R, Fowler N, Guntheroth W. The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 1970;26:480-9. 24. Hazinski M. Cardiovascular disorders. In: Hazinski M, editor. Nursing care of the critically ill child. 2nd ed. St Louis: Mosby; 1992. p. 117-394. 25. Daily E, Schroeder J, editors. Techniques in bedside hemodynamic monitoring. 5th ed. St Louis: Mosby; 1994. 26. Frey B, Butt W. Pulse oximetry for assessment of pulsus paradoxus: a clinical study in children. Intensive Care Med 1998;24:242-6. 27. Slaughter T. The coagulation system and cardiac surgery. In: Estafanous F, Barash P, Reves J, editors. Cardiac anesthesia: principles and clinical practice. Philadelphia: JB Lippincott; 1994. p. 621-33. 28. Emmanouilides G, Reimenschneider T, Aleen H, Gutgesell H, editors. Clinical synopsis of Moss and Adams’ heart disease in infants, children, and adolescents. Baltimore: Williams and Wilkins; 1998. 29. Kern F, Gieser W, Farrell D. Extracorporeal circulation and circulatory assist devices in the pediatric patient. In: Lake C, editor. Cardiac anesthesia. Philadelphia: WB Saunders; 1993. p. 151-79. 30. Andrew M, Paes B, Milner R, Johnston M, Mitchell L, Tollefsen D, et al. Development of the human coagulation system in the full-term infant. Blood 1987;70(1):165-72. 31. Kern F, Morana N, Sears J, Hickey P. Coagulation defects in neonates during cardiopulmonary bypass. Ann Thorac Surg 1992;54:541-6. 32. Grayck E, Meliones J, Kern F. Perioperative issues in other organ systems. In: Chang A, Hanley F, Wernovsky G, Wessel D, editors. Pediatric cardiac intensive care. Baltimore: Williams and Wilkins; 1998. p. 397-407. 33. Vincent R, Elixson E. Hemodynamic monitoring. Crit Care Q 1986;9(2):40-8. 34. Elixson E. Hemodynamic monitoring modalities in pediatric cardiac surgical patients. Crit Care Nurs Clin North Am 1989;1(2):263-73. 35. Bloedel Smith J, Baker A, Moynihan P, Lincoln P, Lawrence Kane P. Cardiovascular critical care problems. In: Curley M, Bloedel Smith J, Moloney-Harmon P, editors. Critical care nursing of infants and children. Philadelphia: WB Saunders; 1996. p. 1100. 36. Keeley S. Hematologic problems. In: Macnab A, Macrae D, Henning R, editors. Care of the critically ill child. New York: Churchill Livingstone; 1999. p. 638. 37. Henning R. Fluid resuscitation in children. Emerg Med 1996;8(1):57-62.
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The incidence of cardiac tamponade after cardiac surgery is reported as ranging from 0.04% to 7%. Although a relatively infrequent complication, tamponade is associated with significant morbidity and mortality. Reports of tamponade after pediatric cardiac surgery are few and generally associated with postcardiotomy syndrome or, less commonly, removal of left atrial or pulmonary artery catheters after surgery. A case is presented of cardiac tamponade in a pediatric patient resulting from removal of a direct atrial and a pulmonary artery catheter after cardiac surgery. The pathophysiology of cardiac tamponade is reviewed and the increased risk for pediatric patients is outlined. The case review is conducted in the context of existing policies in the reporting institution and recommendations for practice are discussed. (Heart Lung® 2000;29:256-61.)
A
cute cardiac tamponade is a rare but lifethreatening complication after cardiac surgery. Tamponade after cardiac surgery may be an early complication in the initial 7-day postoperative period. It may also be a late complication, occurring up to 6 months after surgery.1-3 The time of occurrence may be related to the etiology. Coagulopathies that occur in association with cardiopulmonary bypass combined with inadequate surgical hemostasis are the usual cause of early cardiac tamponade. Although the aortic suture line and atriotomy are common bleeding sites, discrete sites may not necessarily be identified. Early tamponade may also occur as a complication of removal of intracardiac monitoring catheters. In a 10-year review of 6690 intracardiac monitoring catheters in 5666 pediatric patients From the aVictorian Centre for Nursing Practice Research and bRoyal Children’s Hospital. Reprint requests: Linda J. Johnston, RN, BSc, PhD, Senior Research Fellow, The Victorian Centre for Nursing Practice Research, University of Melbourne, Level 1, 723 Swanston St, Carlton, Victoria, 3053 Australia. Copyright © 2000 by Mosby, Inc. 0147-9563/2000/$12.00 + 0 2/1/106208 doi:10.1067/mhl.2000.106208
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undergoing cardiac surgical procedures, an overall bleeding complication rate of 0.22% was identified. Of these patients, 0.04% had an associated tamponade.4 Tamponade has also been described in adults secondary to the removal of epicardial pacing wires.5,6 Although most reports of late tamponade have been described in adults, it has also been described in children after aortopulmonary anastomoses2,7 and occasionally after atrial septal defect repairs and insertion of intra-atrial baffles.2 Late tamponade may occur as a result of postcardiotomy syndrome and anticoagulation therapy.1,2,8 As a complication of postcardiotomy syndrome tamponade is infrequent, yet it is reported more in the pediatric age group than in adults.9 In neonates, tamponade is also a recognized iatrogenic complication of central venous line placement, administration of fluids, or both.10-15
PATHOPHYSIOLOGY The pericardial sac surrounding the heart is composed of fibrous tissue with little elasticity. The sac contains a small volume of fluid that serves to cushion and protect the myocardium.16 The inextensibility of the pericardium means the heart
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Cardiac tamponade after removal of atrial catheters
Fig 1 Major hemodynamic changes and compensatory mechanisms associated with cardiac tamponade. As cardiac output decreases, compensatory mechanisms driven by the sympathetic nervous system are activated. Although the initial response will result in an increase in cardiac output, unalleviated tamponade will eventually overwhelm the compensatory mechanisms. The increase in heart rate increases myocardial oxygen requirements and shortens ventricular filling time leading to an additional decrease in stroke volume and coronary perfusion. Peripheral vasoconstriction may increase afterload to the point that ventricular ejection is compromised. Closed arrows, Succession of events in tamponade; open arrows, compensatory mechanisms.
and pericardial contents compete continuously for a relatively fixed intrapericardial volume. As such, a slow accumulation of fluid may be accommodated by a progressively stretching pericardium. In contrast, rapid accumulation of fluid in the relatively noncompliant surrounds of the pericardium will be at the expense of cardiac chamber volume.3,17-19 If unchecked by the major compensatory mechanisms, the continued compression of the ventricular and atrial volumes will lead to resistance to car-
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diac filling and a progressive reduction in ventricular stroke volume (Fig 1). Classically, tamponade is defined by a group of symptoms known as Beck’s triad: the heart is small and heart sounds are muffled, the venous pressure is elevated, and the systemic arterial pressure is decreased.20 Tamponade is clinically apparent as tachycardia, a narrowed pulse pressure, peripheral vasoconstriction evidenced by clammy, cold extremities and reduced perfusion, and, eventual-
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ly, hypotension.21 Dyspnea, abdominal symptoms, and the sinus tachycardia are the more common symptoms associated with tamponade.22 The condition may also be indicated by pulsus paradoxus. Normally, as intrathoracic pressure decreases during inspiration, right atrial pressure decreases and venous return to the right heart is augmented. Concurrently, the pulmonary vasculature expands, leading to increased venous pooling in the lungs and a subsequent reduction in left ventricular filling, resulting in a decreased stroke volume and a fall in systolic pressure of less than 10 mm Hg.21 The inspiratory decline in systolic pressure is excessive (ie, greater than 10 mm Hg), as the increase in right heart volume because of tamponade increases the intrapericardial pressure even further and transmural (intrapericardial versus intrapleural) pressure falls. This phenomenon of respiratory reciprocation where inspiration increases right heart filling at the expense of left heart filling with reversal on expiration is expressed as pulsus paradoxus.19,20,23 In the patient with positive pressure ventilation, pulsus paradoxus may in fact be reversed.1,24 Positive pulsus paradoxus is identified by an exaggerated rise (>10 mm Hg) in systolic pressure during inspiration.25 It may also be absent in tamponade associated with left ventricular failure, hypovolemia, atrial septal defect, or severe aortic incompetence.21 Pulsus paradoxus may be determined in those patients with an indwelling arterial catheter by observing the decline in systolic blood pressure during the inspiratory cycle. Pulse oximetry may be a noninvasive method for measuring the degree of pulsus paradoxus in the pediatric patient who is not receiving ventilation.26 This measurement, which is technically more challenging to get, is obtained through measuring the respiratorydependent changes of the pulse waveform on the oximeter.
Altered hemostasis in children after cardiac surgery The anticipated response for every patient whose blood has been subjected to the nonendothelialized bypass circuit is a predisposition to clot formation and platelet activation. As such, patients are routinely heparinized during bypass, resulting in an increased risk of excessive bleeding after surgery as a result of the associated disturbed platelet function and fibrinolysis.27,28 In neonates and infants, altered hemostasis is exacerbated by the hemodilution effect resulting from a relatively large circuit prime to small blood volume ratio and
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the severe inflammatory response and release of associated mediators that is magnified by deep hypothermia and circulatory arrest. In addition, there are altered responses to heparinization. These include delayed hepatic clearance and the reduction in the effectiveness of clotting factors as a result of the hemodilution.29 Pediatric patients undergoing cardiac surgery are subject to additional disturbances in hemostasis after cardiopulmonary bypass because of factors related to their being children with congenital heart disease. Altered hepatic function in association with congenital heart disease can occur through low cardiac output, hemodynamic instability, or rarely, inferior vena caval obstruction. Also, in infants up to 6 months of age, immature hepatic synthetic function prolongs the activated partial thromboplastin time.30,31 This immature function is related to decreased levels of contact factors (eg, factor XII, XI, prekallikrein, and high molecular weight kininogen).32 Bleeding is also potentially worse in the presence of cyanotic congenital heart disease because of associated thrombocytopenia and platelet dysfunction.29 Other relevant associations are the use of prostaglandin E, asplenia, technical surgical complexity involving extensive reconstruction and suturing, reoperation through vascular scar, and the resultant prolonged bypass time.32
Monitoring in the pediatric patient after cardiac surgery Invasive hemodynamic monitoring is an essential component of postoperative assessment after pediatric cardiac surgery. One component of this assessment, and one that is common to the pediatric population, is the measurement of pressures via direct transthoracic, intracardiac monitoring catheters. These 19-gauge catheters are easily placed in the heart under direct vision at the time of surgery, secured with a purse-string suture to the epicardium, and exit the mediastinum via the chest wall. Thus unlike in monitoring in the adult patient, pulmonary artery catheters are not routinely used.33,34 The patency of these catheters after surgery is maintained with a heparinized continuous infusion. Right atrial pressure provides a measurement of systemic venous return, vascular volume, and function of right side of the heart. Monitoring of left atrial pressure provides information about pulmonary venous pressure, left ventricular preload and function, and systemic volume. Measurement of pulmonary artery pressure is an indicator of right ventricular function and outflow tract patency, pulmonary vascular reactivity, venous pressure in the
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Table Clotting profile of the patient before removal of direct transthoracic monitoring catheters* Patient (RCH Reference Range)
Fibrinogen (g/L) Platelets (×109/L) PT (s) PTT (s)
4.6 59 16.2 37
(1.5-4) (150-400) (12-16) (27-38)
Accepted in ICU patient
183 161 13.9 63.7
± ± ± ±
33 (% activity) 65 1.7 14.1
PT, Prothrombin time; PTT, partial thromboplastin time. *The Royal Children’s Hospital (RCH) Reference Range and those identified as acceptable in the ICU patient 24 hours after surgery are shown for comparison.32
lungs, and mean filling pressure on the left side of the heart.34,35 Direct intracardiac catheters are generally reserved for hemodynamic monitoring and are removed after the acute postoperative period.
CASE REPORT Baby P was born at term (birth weight, 3.3 kg) by normal vaginal delivery to a gravida 9, para 7 mother. Antenatal ultrasonagraphy suggested a cardiac abnormality and possible Down syndrome. Postnatal chromosome analysis and echocardiography confirmed the genetic diagnosis and revealed a complete atrioventricular septal defect with a small patent ductus arteriosus. With severe failure to thrive and hospitalized since birth, she was transferred to our institution at the age of 6 weeks for surgical intervention and continuation of care. A complete repair was undertaken with a degree of left and right atrioventricular (AV) valve incompetence evident at time of surgery. Pulmonary hypertension and continued ventilator dependence after surgery necessitated additional surgery 13 days later for poor left AV valve function. Both right and left AV valves were revised with some improvement in function. Cardiopulmonary bypass time was 71 minutes, and the patient’s temperature was lowered to 28°C. Pacing wires, a left atrial (LA) catheter, pulmonary artery catheter, Tenckhoff peritoneal catheter, and 2 mediastinal chest drains were inserted per routine, and the patient was transferred to the intensive care unit. The initial course after surgery was unremarkable, and both chest drains were removed on day 2 after minimal drainage in total and no drainage over the preceding 12 hours. On the fourth day after surgery the direct monitoring catheters were removed. Six hours before removal of the catheters
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the associated heparinized infusions were discontinued. A clotting profile revealed a low platelet count, a normal activated partial prothrombin time, prolonged prothrombin time, and an elevated fibrinogen level (Table). Subsequently, 37 mL (10 mL/kg) of platelets was administered 1 hour before removal of the LA catheter. Blood loss from the site after removal was estimated at 15 mL and was associated with a decrease in mean arterial pressure (MAP) from 68 to 40 mm Hg. The administration of 20 mL of 4% albumin resulted in a significant improvement in the MAP to 50 mm Hg. Fifteen minutes later, in consultation with medical staff, the pulmonary artery catheter was removed. Continuous ooze was accompanied by a marked deterioration in the patient’s color, a decrease in MAP to 25 mm Hg, bradycardia, and loss of a pulsatile arterial trace on the monitor. Immediate resuscitation consisted of cardiac compressions, adrenaline, volume expansion, hand ventilation, and needle aspiration of 8 mL bloody fluid from the pericardial space. Subsequently, cardiac tamponade was diagnosed by echocardiography. The sternotomy wound was opened with the patient under general anesthetic in the ICU, and the pericardial space was entered. Approximately 200 mL of blood and clots were removed from the pericardial cavity. Continuous bleeding from the heart muscle was noted at the site of the LA catheter removal and was oversewn with achievement of hemostasis. Physicians completed a standard sternotomy closure and inserted a single chest drain; the infant was in a stable condition. A stormy course after surgery complicated by an inability to wean from the ventilator necessitated plication of the diaphragm and additional mitral and tricuspid valve repair. The infant was trans-
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ferred back to the referring hospital at 31⁄2 months of age with oxygen saturations above 90% in room air (FiO2 0.21); in addition, the infant received diuretics, an angiotensin-converting enzyme inhibitor, sodium supplements, and breastfeeding, but required nasogastric tube feeding supplements.
DISCUSSION Management of the pediatric patient after cardiac surgery varies between institutions. At our institution, hemodynamic monitoring catheters are routinely removed 4 days after surgery when the patient has usually been transferred to the cardiac surgery unit for continued care. Once the decision has been made to stop monitoring, those lines that have had continuous heparinized infusions remain in situ and are turned off for 24 hours before removal. Unit policy dictates that lines are removed (1) during the day when surgeons are available, (2) when the blood coagulation profile is normal (platelets may be administered before removal if indicated), and (3) only with the written order of the surgeon. The technique for removal is one of even, gentle traction followed by continued pressure over the insertion site for a couple of minutes. Any oozing from the site is noted and the dressing reinforced. As the direct atrial lines are sutured into cardiac muscle, the patient is observed closely for signs of bleeding, effusion, or cardiac tamponade. The onset of pallor, tachypnea, and tachycardia are particularly noted. If the child is still in the ICU, heart rate, oxygen saturation, and blood pressure will be continuously monitored. However, in most instances the child will have been transferred to the cardiac surgery unit without continuous monitoring, and an echocardiograph is obtained within hours of catheter removal. Although the use of direct transthoracic monitoring catheters is not a simple undertaking, neither is their removal. Entrapment, bleeding, and tamponade may be associated complications. Death may even result. The removal of direct monitoring catheters on the first or second day after surgery and before removal of chest drains may enable drainage and the detection of such bleeding.4 However, consideration should also be given to the altered hematologic status that may be present in these patients at this relatively early point in the postoperative recovery period as a result of undergoing cardiopulmonary bypass. In the reporting institution, the chest drain is removed when drainage is considered minimal, usually the day
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after surgery. Direct monitoring catheters remain in situ until day 4 after surgery to minimize the risk of bleeding that may be associated with removal. Before removal of direct transthoracic monitoring catheters, it is recommended that crossmatched blood and platelets be available and that patients be checked for coagulopathies and abnormalities corrected. Administration of platelets will normally rectify a coagulopathy, and it is not routine to recheck the platelet count after transfusion. An infusion of 70 mL platelets per 5 kg body weight should increase the count by 50 × 109/L.36 When more than 1 line is being removed simultaneously, as in the case study described, active bleeding at the first site should be treated with a high index of suspicion and the platelet count rechecked. In the case presented, re-exploration of the sternotomy identified the origin of the bleeding as the previous site of the LA catheter, the first catheter to be removed. Compensatory mechanisms in the pediatric patient will maintain the blood pressure initially. Tachycardia and vasoconstriction with cool and mottled extremities will be apparent. It is not until blood loss reaches 30 mL/kg, almost half the total blood volume, that blood pressure will fall.37 In the event of continued bleeding despite previous supposed correction of a coagulopathy, additional blood products and surgical exploration will be required. The nurse caring for the pediatric patient after cardiac surgery must be aware of the signs of impending tamponade. Close observation will identify the tachycardia and pallor associated with an acute and large volume of blood loss before a terminal bradycardia and hypotension eventuate. Identification of the child with a slower accumulation of blood in the pericardial space may be more difficult. Recognition of an increasing hypoxia, sometimes manifested as disorientation or unusual behavior, may be confounded by other factors, such as the developmental age of the child and the psychologic response to hospitalization and the surgery. Clinical decision making should always be based on sound knowledge and informed by current institution policy. Heightened awareness of this rarely seen clinical condition may be promoted by regular education sessions and attendance by nursing staff at scheduled morbidity and mortality meetings. In conclusion, although tamponade in the pediatric patient after cardiac surgery may be a rare occurrence, the nurse caring for these patients should be vigilant in the assessment of this “at-
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risk” patient population and recognition of this complication.
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