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Ann Thorac Surg 1998;66:1242-1245
© 1998 The Society of Thoracic Surgeons


Original articles: cardiovascular

Recognition and management of catheter-induced pulmonary artery rupture

Michael H. Mullerworth, MBBSa, Peter Angelopoulos, BAppSca, Melanie A. Couyant, BSca, Alison M. Horton, CCPa, Susan M. Robinson, MBBSb, Oscar U. Petring, MDb, Peter J. Mitchell, MBBSd, Jeffrey J. Presneill, MBBSc

a Department of Cardiothoracic Surgery, The Royal Melbourne Hospital, Melbourne, Australia
b Department of Anaesthesia, The Royal Melbourne Hospital, Melbourne, Australia
c Department of Intensive Care, The Royal Melbourne Hospital, Melbourne, Australia
d Department of Radiology, The Royal Melbourne Hospital, Melbourne, Australia

Accepted for publication April 19, 1998.

Address correspondence to Dr Mullerworth, Royal Melbourne Hospital, Melbourne, PO Box 2148, 3050, Australia


    Abstract
 Top
 Abstract
 Introduction
 Material and methods
 Comment
 References
 
Background. Catheter-induced pulmonary artery rupture is a well-recognized complication of invasive monitoring, but the risk has not diminished. Although commonly associated with cardiopulmonary bypass, injuries also occur in intensive care. Definitive proof requires pulmonary angiography or autopsy. Many cases are never reported, and lesser injuries are probably underdiagnosed.

Methods. Seven cases fulfilling accepted diagnostic criteria discovered over 2 years are described in four groups illustrating the common modes of presentation: hemoptysis with hypoxemia, exsanguination, delayed recurrent hemorrhage, and bleeding with cardiopulmonary bypass.

Results. One patient had a planned elective operation deferred. Four patients were being monitored in intensive care. Two of them died of pulmonary artery rupture. Two other patients had bleeding on weaning from cardiopulmonary bypass. One settled with conservative treatment, the other survived after extracorporeal life support. Recognition and management are discussed, emphasizing means of avoiding pulmonary resection.

Conclusions. Catheter-induced pulmonary artery rupture is unavoidable. Constant awareness is essential. A plan of management is presented. Extracorporeal life support may help to avoid pulmonary resection. Early pulmonary angiography is advocated for accurate diagnosis and to enable treatment by embolization.


    Introduction
 Top
 Abstract
 Introduction
 Material and methods
 Comment
 References
 
Flow-directed catheters to monitor pulmonary artery (PA) and indirect left atrial pressures were first introduced in 1970 [1] and are now commonly used during cardiac operations and in patients requiring intensive care. Numerous complications have been reported, but most are avoidable [2, 3], and they are rare during investigative right heart catheterization. One serious complication that still occurs is PA rupture; as was suspected many years earlier [2, 4], many cases are probably not being recognized or reported. More recently there have been several reports describing delayed hemorrhage, especially from PA pseudoaneurysms [511]. This article will not address controversies over the indications for PA catheter insertion [12, 13].


    Material and methods
 Top
 Abstract
 Introduction
 Material and methods
 Comment
 References
 
We report 7 cases of PA rupture encountered over 2 years (June 1995 to June 1997), to illustrate options in management. Three of these cases were among 1,500 operations using cardiopulmonary bypass (CPB). One of these patents survived after extracorporeal life support (ECLS). All incidents occurred in a tertiary referral teaching hospital where approximately 750 open heart operations are performed each year, and which has a separate 14-bed general intensive care unit. A heparin-coated thermodilution catheter (model 93A-83H-7.5F, Baxter Laboratories, Santa Ana, CA) was used. Insertion technique and management followed standard guidelines, similar to Stone and coworkers [2]. The modes of presentation and management are summarized in Figure 1. The case of patient 7, being very unusual, is described in more detail:



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Fig 1. Modes of presentation. (CPB = cardiopulmonary bypass; ECLS = extracorporeal life support; ETT = endotracheal tube; ICU = intensive care unit; PAC = pulmonary artery catheter; PEEP = positive end-expiratory pressure.)

 
A woman aged 71 years had triple-vessel coronary artery bypass grafting (CABG) without incident, until she was weaned from CPB. Falling arterial systolic blood pressure (to 40 mm Hg) and arterial oxygen saturation (to 69%), with rising pulmonary inflation pressures, were noted shortly before blood and froth appeared in the endotracheal tube. Cardiopulmonary bypass was resumed; the left lung was normal except for hyperinflation, and the right middle and lower lobes were engorged with intrapulmonary hemorrhage. The PA catheter could not be felt in the right lung hilum. It was withdrawn 5 cm even though it appeared to be well positioned. The airway was cleared with a fiberoptic bronchoscope and no fresh bleeding was seen. After 1 hour of support, she was once again weaned off CPB with intravenous infusions of dopamine and epinephrine. Despite ventilation with 100% oxygen (inspired oxygen fraction, 1.0) and 10 cm H2O positive end-expiratory pressure, she remained hypoxemic in a low cardiac output state (cardiac index, 1.8 L · min-1 · m-2) with metabolic acidosis. Small challenge doses of protamine sulfate were given to exclude an idiosyncratic reaction to protamine, and then the full dose was administered.

Metabolic acidosis and respiratory insufficiency worsened (pH 7.19; arterial oxygen tension, 75 mm Hg; arterial carbon dioxide tension, 50 mm Hg, arterial oxygen saturation, 90%; cardiac index, 2.2 L · min-1 · m-2), and the heart and both lungs became distended. Therefore venoarterial ECLS was begun from the right common femoral artery and vein using Biomedicus percutaneous cannulas 19F arterial and 27F venous, with a Biomedicus BP80 centrifugal pump (Medtronic Cardiopulmonary, Anaheim, CA), a Carmeda circuit, and a Maxima oxygenator (Medtronic Inc, Eden Prairie, MN). The circuit was primed with Plasmalyte 148 (Baxter Healthcare, Old Toongabbie, NSW, Australia) and connected air-free to the cannula. A small loading dose of heparin (5,000 units) was given before slowly building up to a flow rate of 3.5 L/min. It was possible to reduce ventilation parameters as oxygenation and metabolic acidosis improved. The PA catheter was left in place, and was very useful in postoperative care. The PA pressure fell immediately from 40 over 20 to 30 over 20 mm Hg. Preoperative PA pressure was 34 over 20 mm Hg. Subsequently it was kept as low as possible while maintaining adequate circulatory parameters. The edges of the divided sternum could not be approximated, but the superficial soft tissues were closed.

Extracorporeal life support was managed by the perfusion team in the cardiac intensive care unit for the next 50 hours. A heparin infusion was begun 6 hours after starting ECLS, initially at 1,000 U per hour, when there was little continuing blood loss from the chest tubes. This was progressively increased till an activated clotting time measured by Hemotech (Medtronic Hemotech Inc., Englewood, CO) of 200 seconds resulted by the tenth hour. Thereafter it was maintained at 160 to 180 seconds (normal, 90 to 130 seconds, low-range cuvette). The ECLS flow rate was kept at 3.0 to 4.5 L/min until the last few hours, when it was slowed to 1.8 L/min for weaning. No thrombotic or hemorrhagic problems were encountered. On the second postoperative day the patient was returned to the operating room, fully anticoagulated with heparin, and weaned successfully. The perfusion cannulas were removed, the groin vessels repaired, and the sternal edges wired together. Circulation in the right leg was good. Inspection of the right lung showed that the middle and lower lobes were solid and dark purple in color. Ventilatory assistance was continued for a further 10 days through a tracheostomy (inspired oxygen fraction, 0.6; positive end-expiratory pressure, 10 cm H2O), and cardiac inotropic agents were needed for 2 weeks. An echocardiogram at this time showed normal left ventricular function with mild right ventricular dysfunction, and an estimated peak PA pressure of 42 mm Hg. Oral administration of captopril was resumed. Chest radiograph appearances showed progressive clearing to a residual smooth elliptic opacity in the right midzone, thought to be in a lung fissure. A pulmonary angiogram was done 5 weeks after the operation and was normal. The right midzone opacity condensed to a thickening in the right horizontal fissure by 2 months after the operation, and the patient remained well 2 years later, at which time a computed chest tomogram was normal except for minor atelectasis in the middle lobe of the right lung.


    Comment
 Top
 Abstract
 Introduction
 Material and methods
 Comment
 References
 
Pulmonary artery rupture from catheter injury during invasive monitoring is an uncommon but often lethal complication. Comprehensive reviews of the literature have been done [46, 14]. The reported incidence is between 0.2% and 1.0% [2, 6, 14] with a mortality of 50% [4, 6, 8]. Hence it is essential to maintain a high level of suspicion and to have a clear plan of management. Such plans have been formulated previously, covering endobronchial bleeding occurring during preoperative insertion [2, 5, 6] and during CPB [2, 5, 6, 15]. The injury is commonest in elderly women undergoing CPB [2, 4, 6]. Most ruptures occur on the right side [6, 7, 9]. Other predisposing factors are anticoagulation and PA hypertension [5, 6, 8]. The mechanism of injury is damage to the arterial wall either by the advancing catheter tip, or by normal or eccentric balloon inflation, especially when the catheter tip is wedged. Stiffening of the catheter during CPB with hypothermia and displacement of the catheter tip when the heart is manipulated may also be responsible [5, 6, 10, 14]. Preventive measures include proximal positioning and avoidance of fixed wedging of the catheter tip, limiting balloon inflation and avoiding inflation when wedged, and withdrawal of the catheter tip before institution of CPB [2, 4, 5]. A PA catheter should not be inserted as a routine, but preferably only in selected cases when it can be shown to be of value [12, 16]. Although a transesophageal ultrasound probe can be extremely useful intraoperatively, it cannot provide continuing hemodynamic monitoring in the conscious postoperative patient. Of other alternative methods available, there is no consensus on which newer noninvasive technologies are most appropriate for which patients [13, 16].

A management plan for suspected PA rupture is shown in Figure 2. "Warning" hemorrhage may occur soon after insertion, and any planned operation should be deferred [3, 6, 14]. Minor bleeding may cease spontaneously, or will often be controlled by selective bronchial intubation, correction of coagulation deficiencies, and positive end-expiratory pressure, but may recur later (patients 1, 2, and 6). The case of patient 6 illustrates the risk of delayed massive hemorrhage caused by rupture of a false aneurysm. Rebleeding occurs in 45% of such cases [6], and has been described from 48 hours to 14 days later [6]. Survival of the short-term hemorrhage should be followed by early investigation for a possible pseudoaneurysm, even with nominal hemoptysis and without chest radiographic abnormality [8, 11]. Persisting focal abnormalities in chest radiographs should raise suspicion, but may initially be indistinguishable from pulmonary infarction or hemorrhage [5, 9]. Computed tomography with intravascular radiopaque contrast or, preferably, a pulmonary angiogram is recommended, followed by transcatheter embolization [69, 17]. "Do not watch and wait" might be the best advice [9, 10] because one cannot be certain that there will be spontaneous healing. In retrospect angiography should have been done as soon as possible in patient 7 to obviate this risk.



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Fig 2. Treatment algorithm for suspected pulmonary artery rupture. Flow diagram for plan of management. (CPB = cardiopulmonary bypass; ECLS = extracorporeal life support; ETT = endotracheal tube; PAC = pulmonary artery catheter; PEEP = positive end-expiratory pressure.)

 
It is frequently assumed that PA injuries will resolve completely with conservative management, but the natural history of PA rupture is not clear or uniform. Some injuries certainly heal without apparent trace but others progress to pseudoaneurysm and rupture. Therefore it would seem necessary to investigate all patients, not only those who have survived large hemorrhages, and to do careful autopsies, to identify any predictive signs. When bleeding occurs during CPB, commonly when the lungs are ventilated during weaning from extracorporeal circulation [6, 10, 15], full CPB should be resumed to reduce pulmonary blood flow and pressure and to control bleeding. Venting of the PA may further assist in identifying the bleeding site by bronchoscopy [15], followed by isolation of that part of the airway [4, 6, 15]. This may be followed, if possible, by direct arterial repair [18] or by pulmonary resection [4, 19, 22, 23]. When there is extensive intrapulmonary hemorrhage, arterial repair is usually not possible, but temporary control of the ipsilateral PA may help [19, 20]. However, lobectomy or even pneumonectomy may be the only alternative, especially when bleeding occurs freely into the pleural space [4, 6, 19].

Pulmonary resection in the setting of a cardiac operation with CPB increases morbidity and mortality [6, 21]. Loss of lung tissue may compromise gas exchange more than ventilation–perfusion mismatch, and may not avoid the need for subsequent circulatory or ventilatory assistance, even after arterial repair alone [18]. We elected to use ECLS in patient 7 because external assistance was clearly required, and also because it offered a chance to avoid lung resection. Full CPB uniformly diminishes or arrests bleeding from the pulmonary circulation [5, 6, 10, 15], and ECLS should do the same provided adequate flows are achieved. Although low-level anticoagulation increased the risk of fresh hemorrhage, we believe that stabilization of the patient’s circulation and ventilation, and reduction of PA pressure, achieved a satisfactory outcome. Controlled ventilation helps avoid straining and coughing [14]. The ECLS system allowed flows to match venous drainage, thereby preventing overload of the pulmonary circulation, and also maintained systemic arterial perfusion and oxygenation.

Life-threatening bleeding still occurs [22, 23], and we agree that pulmonary resection is effective treatment, but that may not be the only way to reduce morbidity and mortality. When limited pulmonary reserve precludes resection one alternative is PA occlusion with a vascular loop for up to 2 days [19, 20].

Another alternative is ECLS, which was successful in patient 7. However, it must be conceded that the risk of rebleeding remains if the bleeding site has not been surgically controlled by arterial repair or by lung resection.

Even so, the technical difficulties and risks of pulmonary resection combined with other major (especially cardiac) surgical procedures are not small and should be avoided. Transcatheter embolization is probably preferable wherever possible.

In conclusion, prevention, recognition, and management of catheter-induced PA rupture has been well described previously in a number of different situations. In spite of comprehensive guidelines and catheter modifications, this complication is not always avoidable. The following points require reemphasis:

  1. Maintain a high level of suspicion. Any airway bleeding with a PA catheter in situ is a cause for concern.
  2. Cases may present not with endobronchial hemorrhage but with unexplained hypovolemic collapse, respiratory embarrassment, or hemothorax.
  3. The absence of radiologic changes in the lungs does not guarantee the absence of arterial injury, but focal opacities should raise concern.
  4. Pulmonary resection should be avoided except when catastrophic free bleeding into a pleural space cannot be controlled.
  5. Particularly in the operating room setting, ECLS offers an additional means of overcoming pulmonary and circulatory insufficiency, reducing the risk of recurrent bleeding, and avoiding pulmonary resection.
  6. All survivors of short-term hemorrhage should have early investigation for possible pseudoaneurysm. At present it is not possible to predict which injuries are potentially lethal. Transcatheter embolization may be life-saving and may also preserve more function than lung resection.


    References
 Top
 Abstract
 Introduction
 Material and methods
 Comment
 References
 

  1. Swan H.J.C., Ganz W., Forrester J., Marcus H., Diamond G., Chonette D. Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. N Engl J Med 1970;283:447-451.
  2. Stone J.G., Khambatta H.J., McDaniel D.D. Catheter-induced pulmonary arterial trauma: can it always be averted?. J Thorac Cardiovasc Surg 1983;86:146-150.[Abstract]
  3. Barash P.G., Nardi D., Hammond G., et al. Catheter-induced pulmonary artery perforation. J Thorac Cardiovasc Surg 1981;82:5-12.[Abstract]
  4. Kelly T.F., Morris G.C., Crawford E.S., Espada R., Howell J.F. Perforation of the pulmonary artery with Swan-Ganz catheters: Diagnosis and surgical management. Ann Surg 1981;193:686-692.[Medline]
  5. Carlson T.A., Goldenberg I.F., Murray P.D., et al. Catheter-induced delayed recurrent pulmonary artery hemorrhage. JAMA 1989;261:1943-1945.[Abstract/Free Full Text]
  6. Urschel J.D., Myerowitz P.D. Catheter-induced pulmonary artery rupture in the setting of cardiopulmonary bypass. Ann Thorac Surg 1993;56:585-589.[Abstract]
  7. Davis S.D., Neithamer C.D., Schreiber T.S., Sos T.A. False pulmonary artery aneurysm induced by Swan-Ganz catheter: diagnosis and embolotherapy. Radiology 1987;164:741-742.[Abstract/Free Full Text]
  8. Dieden J.D., Friloux L.A., III, Renner J.W. Pulmonary artery false aneurysms secondary to Swan-Ganz pulmonary artery catheters. AJR Am J Roentgenol 1987;149:901-906.[Abstract/Free Full Text]
  9. Kirton O.C., Varon A.J., Henry R.P., Civetta J.M. Flow-directed, pulmonary artery catheter-induced pseudoaneurysm: urgent diagnosis and endovascular obliteration. Crit Care Med 1992;20:1178-1180.[Medline]
  10. Cicenia J., Shapira N., Jones M. Massive hemoptysis after coronary artery bypass grafting. Chest 1996;109:267-270.[Free Full Text]
  11. Yellin L.B., Filler J.J., Barnette R.E. Nominal hemoptysis heralds pseudoaneurysm induced by a pulmonary artery catheter. Anesthesiology 1991;74:370-373.[Medline]
  12. Fink M.P. The flow-directed, pulmonary artery catheter and outcome in critically ill patients: have we heard the last word?. Crit Care Med 1997;25:902-903.[Medline]
  13. Peruzzi W.T. Hemodynamic monitoring: does the end justify the means?. Crit Care Med 1997;25:1767-1768.[Medline]
  14. McDaniel D.D., Stone J.G., Faltas A.N., et al. Catheter-induced pulmonary artery hemorrhage. J Thorac Cardiovasc Surg 1981;82:1-4.[Abstract]
  15. Purut C.M., Scott S.M., Parham J.V., Smith P.K. Intraoperative management of severe endobronchial hemorrhage. Ann Thorac Surg 1991;51:304-306.[Abstract]
  16. Sprung C.L., Eidelman L.A. Editorial overview: Cardiopulmonary monitoring. Curr Opin Crit Care 1997;3:219-220.
  17. Feng W.C., Singh A.K. Management of endobronchial hemorrhage [Letter]. Ann Thorac Surg 1991;51:1045-1046.[Medline]
  18. Urschel J.D., Parrott J.C.W. Repair of catheter-induced perforation of the pulmonary artery [Letter]. Ann Thorac Surg 1991;51:1046.
  19. Pellegrini R.V., Marcelli G., DiMarco R.F., Bekoe S., Grant K., Marrangoni A.G. Swan-Ganz catheter-induced pulmonary hemorrhage. J Cardiovasc Surg 1987;28:646-649.[Medline]
  20. Stone J.G., Faltas A.N., Khambatta H.J., Hyman A.L., Malm J.R. Temporary unilateral pulmonary artery occlusion: a method for controlling Swan-Ganz catheter-induced hemoptysis. Ann Thorac Surg 1984;37:508-510.[Abstract]
  21. Tyers G.F.O. Invited commentary on intraoperative management of severe endobronchial hemorrhage. Ann Thorac Surg 1991;51:306-307.
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  23. Sekkal S., Cornu E., Christides C., et al. Swan-Ganz catheter induced pulmonary artery perforation during cardiac surgery concerning two cases. J Cardiovasc Surg 1996;37:313-317.[Medline]



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