Ann Thorac Surg 1998;65:827-829
© 1998 The Society of Thoracic Surgeons
Case Reports
Induced Hypothermia in Critical Respiratory Failure After Lung Transplantation
Leif T. Eriksson, MD,
Stig Steen, MD, PhD
Department of Respiratory Medicine, University Hospital, Lund, Sweden
Department of Cardiothoracic Surgery, University Hospital, Lund, Sweden
Accepted for publication October 9, 1997.
Dr Eriksson, Department of Respiratory Medicine, University Hospital, S-221 85 Lund, Sweden (e-mail: leif.eriksson@lung.lu.se).
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Abstract
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Primary graft failure after lung transplantation is a serious complication with high mortality. We present 2 cases of critical respiratory failure after lung transplantation treated with surface cooling to 32° and 35°C, respectively, as an adjunct to conventional intensive care. Both patients were discharged from the hospital in good clinical condition. Surface cooling may be an effective mode of treatment in patients with critical respiratory failure after lung transplantation and should be considered before extracorporeal membrane oxygenation treatment is initiated.
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Introduction
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Graft failure in the early postoperative period after lung transplantation accounts for about 25% of deaths occurring within 30 days [1]. The cause of this graft failure is often reversible, the problem being to sustain the patient until a diagnosis is made and treatment has been effective. Treatment options when conventional intensive care fails include retransplantation and extracorporeal membrane oxygenation (ECMO). We have successfully treated 2 patients fulfilling accepted ECMO criteria [2] with another treatment option, namely, induced hypothermia. The aim of this report is to present these cases and to discuss induced hypothermia in the treatment of critical respiratory failure after lung transplantation.
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Case Reports
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Patient 1
A 41-year-old woman with Eisenmenger’s syndrome due to a ventricular septal defect underwent a right single-lung transplantation combined with correction of the ventricular septal defect with a patch. During the first postoperative day she had to be reoperated on because of bleeding from the right pleura. Back in the intensive care unit massive pulmonary infiltrates developed on the chest roentgenogram, lung compliance decreased, and the inspired oxygen fraction (FiO2) had to be increased to 1.0 to keep the arterial oxygen tension greater than 60 mm Hg. No CO2 retention was noted. The condition was interpreted as secondary to the operative trauma combined with massive blood transfusions. Her condition stabilized after dehydration, and FiO2 could be reduced to 0.4. On the sixth postoperative day she suddenly deteriorated with increased pulmonary artery pressure, a body temperature of 39°C, and increasing pulmonary infiltrates on the chest roentgenogram. She was hypoxic with CO2 retention and acidosis in spite of an FiO2 of 1.0 and high airway pressures. She fulfilled the criteria for initiating ECMO, but the decision was made to lower her body temperature to 35°C by surface cooling. Buffer treatment was given to keep pH greater than 7.2. The CO2 production decreased by 30% (Fig 1). Treatment with high doses of glucocorticosteroids was given on the suspicion of rejection. Over the next 8 hours her arterial CO2 tension normalized and the FiO2 could be reduced after another 12 hours. Her clinical condition gradually improved, but she needed ventilatory support for another 4 weeks. She was discharged from the hospital 3 months after the transplantation in good clinical condition with normal arterial blood gases.
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(Patient 1.) Postoperative day 6 to 8 measurements of arterial carbon dioxide tension (PaCO2), arterial oxygen tension (PaO2), carbon dioxide production (CO2-prod), inspired oxygen fraction (FiO2), and pH in arterial blood. Arterial blood gases and pH are measured at 37°C and not corrected for body temperature according to the  -stat concept.
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Patient 2
A 55-year-old woman with pulmonary hypertension secondary to chronic pulmonary embolism underwent double-lung transplantation. There was massive intraoperative bleeding. In the intensive care unit her condition was initially stable, but renal insufficiency developed on the third day after the operation. Hemodialysis was started. Her circulation was hyperkinetic with a cardiac output around 10 L/min. This was treated with metoprolol (Seloken, Hässle, Sweden). She was in a stable condition with ventilator support until the 14th postoperative day, when she suddenly deteriorated. Chest roentgenograms showed bilateral infiltrates. Her FiO2 had to be increased to 1.0, and hypercapnia and acidosis developed. Her body temperature was lowered from normothermia to 32°C by surface cooling. Buffer was given to keep pH greater than 7.2. Antirejection therapy with high-dose glucocorticosteroids was given. The patient was kept hypothermic for 4 days; after that the chest roentgenogram cleared and the FiO2 could be reduced to 0.5. She had to be ventilated for another 12 days. She was discharged from the hospital 5 months after the transplantation in good clinical condition with normal arterial blood gases.
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Comment
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The patients presented had critical respiratory failure after lung transplantation and were hypoxemic and hypercapnic with respiratory acidosis, in spite of maximal ventilatory support with an FiO2 of 1.0 and a positive end-expiratory pressure greater than 5 cm H2O. Deterioration was rapid and occurred on the 6th and 14th postoperative day, respectively, a time when the immediate effects of reperfusion have normally abated. The patients fulfilled accepted criteria for initiation of ECMO. They were heavily immunosuppressed, and bacterial infection is common in the period immediately after lung transplantation.
Previous studies on ECMO after lung transplantation have shown a high mortality. In one study where ECMO was used after heart or lung transplantation [3], only 4 of 10 patients survived to leave the hospital. In another study after lung transplantation, 7 of 10 patients survived early graft failure (<7 days) but none of 6 survived late failure (>7 days) [4].
Instead of ECMO, we decided to induce hypothermia in our patients. The rationale for this in critical respiratory failure is to reduce the metabolic rate and thereby oxygen consumption and carbon dioxide production. In the cases presented here a marked effect on gas exchange as a result of the hypothermic regimen could be seen. When temperature was decreased from 39°C to 35°C in the first patient, CO2 production decreased by about 30%.
The pH was kept higher than 7.2 by isotonic buffering (bicarbonate, trometamol) with the intention of keeping pulmonary vascular resistance low [5]. If severe hypercapnia develops in spite of optimal mechanical ventilation, buffer therapy will prevent life-threatening respiratory acidosis [6]. Buffering may allow a decrease in inspiratory pressure and ventilatory volume without the pH approaching potentially dangerous levels [7].
If the patient has severe heart failure, hypothermia should be used with caution because of the increase in vascular resistance it causes and the vascular resistance should be kept low with vasodilating regimens, which will also increase the efficacy of surface cooling. Heavy sedation and complete muscle relaxation are mandatory during the period when the patient’s body temperature is decreased; otherwise, increased sympathetic activity and shivering will increase O2 consumption and CO2 production, even though a reduction in temperature may be achieved. The shivering may not always be clinically apparent.
We have used this concept in 2 other patients in whom respiratory failure developed in the immediate postoperative period after lung transplantation with good results. Several other patients referred to us for ECMO treatment have also been cooled to 32° to 33°C in this manner. The immediate need for ECMO has thus been eliminated and treatment of the underlying cause for the respiratory failure could be initiated. Four patients with adult respiratory distress syndrome have recovered without the need for ECMO.
Hypothermia can be used in conjunction with ECMO treatment [8]; the extracorporeal blood flow can thereby be significantly reduced without deterioration of blood gas values and there is less injury to the blood by the ECMO system.
In conclusion, induced hypothermia combined with heavy sedation, complete muscle relaxation, and buffering may be an effective mode of treatment in patients with critical respiratory failure and can be an alternative treatment to ECMO.
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Acknowledgments
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This study was supported by the Swedish Heart Lung Foundation.
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References
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- Hosenpud JD, Bennett LE, Keck BM, Fiol B, Novick RJ The Registry of the International Society for Heart and Lung Transplantation: Fourteenth official report—1997. J Heart Lung Transplant 1997;16:691-712.[Medline]
- Zapol WM, Snider MT, Hill JD, et al. Extracorporeal membrane oxygenation in severe acute respiratory failure. JAMA 1979;242:2193-2196.[Abstract/Free Full Text]
- Whyte RI, Deeb MG, McCurry KR, Andersson HL, Bolling SF, Bartlett RH Extracorporeal life support after heart or lung transplantation. Ann Thorac Surg 1994;58:754-759.[Abstract]
- Glassman LR, Keenan RJ, Fabrizio MC, et al. Extracorporeal membrane oxygenation as an adjunct treatment for primary graft failure in adult lung transplant recipients. J Thorac Cardiovasc Surg 1995;110:723-727.[Abstract/Free Full Text]
- Wetterberg T, Sjöberg T, Steen S Effects of hypothermia with and without buffering in hypercapnia and hypercapnic hypoxemia. Acta Anaesthesiol Scand 1994;38:293-299.[Medline]
- Wetterberg T, Steen S Combined use of hypothermia and buffering in the treatment of critical respiratory failure. Acta Anaesthesiol Scand 1992;36:490-492.[Medline]
- Menitove SM, Goldring RM Combined ventilatory and bicarbonate strategy in the management of status asthmaticus. Am J Med 1983;74:898-901.[Medline]
- Wetterberg T, Steen S Total extracorporeal lung assist—a new clinical approach. Intensive Care Med 1991;17:73-77.[Medline]
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