Anesth Analg 2001;93:292-293
© 2001 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Respiratory Failure After Pneumonectomy in a Patient with Unknown Hyperlipidemia
Aggeliki Bairaktari, MD,
Bogdan Raitsiou, MD,
Maria Kokolaki, MD,
Maria Mitselou, MD,
Giannis Dritsas, MD,
Gabriel Dahabre, MD, and
Maria Vafiadou, MD
Department of Anaesthesia and Thoracic Surgery, Sismanoglion General Hospital, Athens, Greece
Address correspondence and reprint requests to Aggeliki Bairaktari, 46-48 Kerasoundos Street, 15771 Athens, Greece.
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Abstract
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IMPLICATIONS: We report the case of a patient who had increased lipids in his blood and who complained of dyspnea the first postoperative day after resection of his left lung. As the blood lipids were decreased, his respiration was improved. We conclude that when respiration deteriorates postoperatively, increased blood lipids should be considered as a cause.
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Introduction
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Respiratory failure can occur after pneumonectomy, the usual causes being acute right-sided heart failure, sepsis, arrhythmias, and postoperative pain. Postoperative pain can cause respiratory failure because the patient avoids breathing deeply and coughing, and there may be secretions retained in the remaining lung as well as atelectasis. We report the case of a patient with unknown hyperlipidemia who developed respiratory failure after pneumonectomy.
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Case Report
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A 52-yr-old man was admitted for elective left pneumonectomy because of lung cancer. The patient was mildly obese (82 kg) and a smoker (30 packs per yr) and had myocardial angina 2 yr previously that had been treated with ß-adrenergic blockers for 1 yr. He had adequate exercise tolerance and was free of cardiac symptoms. Preoperatively, forced expiratory volume in the first second and forced vital capacity were within the normal range, with an FIO2 of 0.2, pHa 7.38, PaCO2 36 mm Hg, PaO2 91 mm Hg, base deficit -3 mmol/L, and there was right bundle branch block on the electrocardiogram. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 3 µg/kg, and cis-atracurium 0.15 mg/kg IV. Anesthesia was maintained with 60% N2O in O2 and 1% propofol 4 mg · kg-1 · h-1. Additional doses of fentanyl and atracurium were given according to the needs of the patient. One hour later, the blood in the surgical field became milky. The thoracic surgeon thought at first that lymph fluid had mixed with the blood. The blood continued to be milky, and because the surgeon was sure that he had not caused any damage to the lymph vessels, we decided to stop the infusion of propofol, substituting sevoflurane 1.5%–2% inspired concentrations. After propofol had been given for 105 min and the total amount reached 760 mg, we took a blood sample for measurement of triglyceride and cholesterol levels that showed that the triglyceride level was 152 mmol/L (normal range 0.7–1.9 mmol/L), whereas the cholesterol level was normal. Two hours later the triglyceride level was 81 mmol/L. The patient was tracheally extubated immediately after the operation and later transferred to the ward. On the day of the operation his arterial blood sample showed pHa 7.3–7.36, PaO2 90–110 mm Hg, PaCO2 46–50 mm Hg, and a FIO2 of 0.4. On the first postoperative day the triglyceride level was 79 mmol/L. The patient complained of dyspnea, which worsened. His arterial blood sample showed pHa 7.3, PaO2 55 mm Hg, and PaCO2 48 mm Hg, with FIO2 of 0.5. After endotracheal intubation he was transferred to the intensive care unit. On the second postoperative day, the triglyceride levels continued to be increased (80 mmol/L) and the PaO2 was 60 mm Hg with a FIO2 of 0.8. Therefore, a plasma exchange was performed that decreased the triglyceride to 60 mmol/L. Another two plasma exchanges were performed resulting in decreased triglycerides (20 mmol/L). As the triglycerides decreased, pulmonary function improved and the PaO2 gradually increased (PaO2 79 mm Hg, FIO2 0.5). The trachea was extubated on the fifth day. Respiratory failure attributable to increased lipid concentration was considered the possible cause of the respiratory failure because of the temporal relationship between improvement in respiratory function and the gradual decrease in triglyceride levels (Fig. 1). Other causes, such as myocardial ischemia and acute right-sided heart failure, were excluded with the help of electrocardiography, myocardial enzymes, and pulmonary artery catheter. The patient was hemodynamically stable with arterial blood pressure 100/60–175/110 mm Hg, heart rate 65–120 bpm with few supraventricular and ventricular extrasystoles. The central venous pressure was 9–12 mm Hg and mean pulmonary pressure 12–17 mm Hg. Atelectasis was also excluded with a computed tomography scan of the remaining lung. The patient’s preoperative triglyceride level was 76 mmol/L.
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Figure 1. Relationship between triglyceride plasma levels and PaO2. At a triglyceride level of 79 and FIO2 of 0.5, the PaO2 was 55. At a triglyceride level of 80 and FIO2 of 0.8, the PaO2 was 60. At a triglyceride level of 20 and FIO2 of 0.5, the PaO2 was 79.
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Discussion
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Propofol is formulated as a soya been emulsion and 1 mL propofol 1% contains 0.5 g lipids. Many studies have examined the changes of triglyceride concentrations in a patient receiving prolonged infusions of propofol. Gottaris et al. (1) studied changes in serum lipid concentrations in 10 patients receiving propofol (approximately 33 µg · kg-1 · min-1) over 3 days. No significant increases in triglyceride or cholesterol occurred. In contrast, in another study, 10 of 22 patients sedated with propofol infusion (mean infusion rate of 39 µg · kg-1 · min-1) experienced a doubling of their triglyceride levels after 3 days (2). However, inpatients receiving short infusions of propofol, there is only a temporary increase of triglyceride levels. High blood lipids are associated with an increased risk of respiratory failure as a result of V/Q changes, especially in cases of preexisting lung injury (3–5). Most of these results came from IV fat emulsion administrations in clinical and experimental studies. Although the mechanism is unclear, it is supposed that embolizations of fat particles to the lungs and the release of free fatty acids from the lipids are important steps in the development of respiratory failure. In our case, respiratory failure resulting from increased lipid levels seems the most possible cause of impaired respiratory function.
We conclude that when respiratory function deteriorates postoperatively increased lipid concentrations should be considered as a cause, especially in patients with preexisting pulmonary disease.
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References
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Gottardis M, Khunl-Brady KS, Koller W, et al. Effect of prolonged sedation with propofol on serum triglyceride and cholesterol concentrations. Br J Anaesth 1989; 62: 393–6.[Abstract/Free Full Text]
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Carrasko G, Molina R, Costa J, et al. Propofol vs midazolam in short-, medium-, and long-term sedation of critically ill patients. Chest 1993; 103: 557–64.[Abstract/Free Full Text]
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Hageman JR, Hunt CE. Fat emulsions and lung function. Clin Chest Med 1986; 7: 69–77.[ISI][Medline]
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Greene HL, Hazlett D, Demaree R. Relationship between Intralipid-induced hyperlipemia and pulmonary funtion. Am J Clin Nutr 1976; 29: 127–35.[Abstract/Free Full Text]
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Kimura T, Toung JK, Margolis S, et al. Respiratory failure in acute pancreatitis: a possible role for triglycerides. Ann Surg 1979; 189: 509–14.[ISI][Medline]
Accepted for publication April 11, 2001.
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S.-L. Guo, A. Bairaktari, and S. Ishikawa
Respiratory Failure After Pneumonectomy in a Patient with Unknown Hyperlipidemia * Response
Anesth. Analg.,
June 1, 2002;
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1672 - 1673.
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Abstract
Introduction
