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Morphine-induced acute lung injury
Journal of Clinical Anesthesia (2008) 20, 300–303
Case report
Morphine-induced acute lung injury Christian Hainer MD (Staff Anesthesiologist)a , Moritz N. Wente MD, MSc (Staff Surgeon)b , Peter J. Hallscheidt MD (Professor)c , Jan Schmidt MD (Professor)b , Eike Martin MD (Professor and Chairman)a , Markus W. Büchler MD (Professor and Chairman)b , Markus A. Weigand MD (Professor)a,⁎ a
Department of Anaesthesiology, University of Heidelberg, D-69120 Heidelberg, Germany Department of Surgery, University of Heidelberg, D-69120 Heidelberg, Germany c Department of Diagnostic Radiology, University of Heidelberg, D-69120 Heidelberg, Germany b
Received 20 December 2006; revised 18 October 2007; accepted 24 October 2007
Keywords: Acute lung injury; Morphine; Postoperative care
Abstract A 38-year-old woman who had familial adenomatous polyposis was admitted to the intensive care unit with an episode of severe sepsis 5 days after undergoing a pancreas-preserving duodenectomy. Laparotomy with removal of an intra-abdominal abscess, followed by closed postoperative continuous lavage for 10 days, was performed. During two courses of planned tracheal extubation, the patient developed an acute lung injury, making a reintubation necessary. In both events, the patient received small doses of continuous morphine before the extubation. Morphine may induce the development of an acute lung injury in patients, whereas the exact pathophysiologic and pharmacologic mechanisms remain unclear. © 2008 Elsevier Inc. All rights reserved.
1. Introduction Morphine is still the most widely used analgesic in the intensive care unit (ICU) worldwide. Although the summary of product characteristics for morphine points out that “noncardiogenic pulmonary edema has been observed in intensive-care patients,” very few reports about this issue can be found in the scientific literature [1,2]. In addition to opioid-induced acute lung injury (ALI), there are a number of publications on the occurrence of pulmonary edema after The first two authors contributed equally to the preparation of the article. ⁎ Corresponding author. Tel.: +49 6221 56 6350; fax: +49 6221 56 5345. E-mail address: [email protected] (M.A. Weigand). 0952-8180/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.jclinane.2007.10.017
heroin intoxication and administration of naloxone and buprenorphine [3-11]. The exact mechanisms of these effects are not yet fully understood; opioid-induced ALI occurring approximately two to 4 hours after drug intake is characterized by dyspnea, significant hypoxia, and bilateral infiltrates [12]. Clinical remission is quickly achieved when the triggering substance is eliminated, with the pathologic radiograph changes receding more slowly than the clinical symptoms [13]. Elimination of the harmful substance is the primary objective in the treatment of opioid-induced ALI. Subsequent treatment will depend on the severity of the hypoxia and should follow treatment protocols as published by the Adult Respiratory Distress (ARDS) Network [14-16].
Morphine-induced acute lung injury
301
2. Case report Five days after undergoing a pancreas-preserving duodenectomy, a 38 year-old woman who had familial adenomatous polyposis (FAP) was admitted to the ICU with severe signs of sepsis [17]. She received empirical therapy with imipenem/cilastatin. Computed abdominal tomography (CT) showed signs of an intra-abdominal abscess. Emergency laparotomy showed biliary ascites with no direct signs of an anastomotic insufficiency, but with signs of a putative former leakage via the anastomosis between the neoduodenum and biliary tract and the pancreas, respectively. After extensive lavage, irrigation-suction drains were placed. Then postoperative closed continuous lavage was administered. The patient required mechanical ventilation with an inspired oxygen concentration (FIO2) of 0.5 (PaO2/FIO2 235) and continuous norepinephrine (0.15 μg/kg body weight per min). Before receiving mechanical ventilation, the patient was sedated with propofol/sufentanil (1.9 μg/kg body weight per hr). The intra-abdominal smear showed Enterobacter faecium and Candida glabrata; therefore, antibiotic therapy was augmented with vancomycin and caspofungin. The values for the infection parameters subsequently improved, and the continuous dose of initially required norepinephrine was then gradually reduced. During daily sedation withdrawal, the patient showed agitated-anxious behavior based on a history of anxiety disorders. On day 5 after the patient's admission to the ICU, the analgesic treatment was switched from sufentanil to morphine (0.1 mg/kg body weight per hr). Three hours later,
Fig. 1 Chest radiograph showing poorly defined ground glass opacities involving the lower lung zones.
Fig. 2 Chest radiograph showing bilateral areas of consolidation involving mainly the regions of the lower lobes.
after a successful spontaneous breathing trial, the patient's trachea was successfully extubated. Approximately one hour after extubation, the patient's oxygen demand increased significantly; she then subjectively experienced increasing dyspnea. Despite noninvasive ventilation with the pressure support ventilation mode (inspiratory pressure support 18 cm H2O, positive end-expiratory pressure of 8 cm H2O, with a terminal FIO2 of 1.0), respiratory insufficiency worsened (Fig. 1). Three hours after extubation, reintubation was required. A transthoracic echocardiogram (TTE; normal biventricular systolic and diastolic function, no regional wall motion abnormalities, no right ventricular enlargement, and no paradoxic septum motion) excluded pulmonary embolism or cardiogenic pulmonary edema (CPE). The subsequent chest radiograph showed cloudiness on both sides (Fig. 2). A bronchoscopy was performed to verify or exclude a potential aspiration. As PaO2 decreased further to 44 mmHg, nitric oxide inhalation at 5 ppm was started. With the patient placed in the prone position so as to induce deep sedation and comfort with the respirator, light analgesia with morphine was replaced by sufentanil/midazolam. After two hours, the pulmonary situation improved to the point that the respiratory parameter values could be reduced (FIO2, 0.5; positive end-expiratory pressure, 10 mbar; positive inspiratory pressure, 25 mbar; respiratory rate, 16 breaths per minute) and the supply of norepinephrine was discontinued. Another chest radiograph showed markedly reduced cloudiness. In the afternoon, a thoracic spiral CT scan showed peribronchial consolidation in both lower lobes; the abdominal CT showed fluid collections leading to relaparotomy. Intraoperatively, two hematomas were lavaged; again, there was no indication of anastomotic insufficiency.
302
Fig. 3 Computed tomography of the chest showing patchy peripheral and bronchial consolidation with patchy ground glass of the right and left lower lobe; in addition, a small left anterior pneumothorax was diagnosed.
The following day, sedation was reduced and pressure support ventilation was restarted. On day 3, the patient was switched again from sufentanil to morphine. After 4 hours, the patient once again reported increased dyspnea, with parallel worsening of blood gas values. Thoracic radiograph showed again an incipient pulmonary edema (Fig. 4). At an FIO2 of 0.7 with the patient in prone position, the sedation was again switched from morphine to sufentanil/midazolam. Complete resolution of the situation was achieved within 6 hours. No change in infection parameters was observed. After an intensive chart review, morphineinduced ALI was now suspected; the patient received no further exposure to that substance. On the next day, an uncomplicated percutaneous dilational tracheotomy was performed. The patient was able to start weaning from ventilation over the next several days. Eight days later, the tracheotomy cannula was removed. The patient was fully stable without the need for oxygen.
C. Hainer et al. from CPE. In some situations, the severity of the hypoxia can assist in distinguishing between ARDS/ALI and CPE. In the early stages of ARDS/ALI, hypoxia is often more pronounced than the radiologic pathology would suggest, whereas the radiologic pathology dominates over hypoxemia in the early stages of CPE. In the present case, the patient exhibited an increase in oxygen demand with a saturation of 88% but only minor pathologic radiologic signs (Fig. 1). The radiograph taken two hours later clearly showed bihilar infiltrates (Fig. 2). A radiograph is not a reliable adjunct for distinguishing between ARDS and CPE. Cardiogenic pulmonary edema could be excluded by TTE, because the prevailing acoustic conditions were very favorable. Both the left and right ventricles showed good function. In the absence of any signs of right ventricular overload and diastolic dysfunction, acute pulmonary edema also could be ruled out. In spite of the patient's poor respiratory situation, a bronchoscopy was performed to rule out aspiration as a causative factor. The bronchial system was largely without pathologic findings, with the exception of a moderate amount of glassy secretion. A thoracic/abdominal CT scan was performed approximately 16 hours after the acute event. Two artifacts were found below the abdominal wall, which were removed surgically three hours later and identified as noninfected hematomas. Thoracic CT scan showed bilateral striated, partly spotty dense areas; the small ventral pneumothorax in the left thoracic cavity was treated by insertion of a chest tube (Fig. 3). The subsequent rapid remission of the clinical situation was remarkable. The radiograph also showed evidence of surprising improvement (Fig. 4). Three
3. Discussion Patients in ICUs are at high risk for drug side effects and interactions. In this report, we present a case of morphineinduced ALI. Adult respiratory distress syndrome and ALI can occur from a wide diversity of associated conditions, with sepsis being the most common cause. Multiple transfusions, severe trauma, lung contusion, and aspiration of gastric acid are also independent risk factors for ARDS and ALI. The clinical syndromes have to be differentiated
Fig. 4 Chest radiograph after second episode of morphineinduced unspecific acute lung injury, with almost complete recovery.
Morphine-induced acute lung injury days after the acute event, a very similar situation arose. Again, morphine had been administered to support the weaning process. This was the situation in which druginduced ALI was first considered as a differential diagnosis. Other possible causes, such as acute bronchial obstruction or negative pressure pulmonary edema, were ruled out by clinical observation. On closer differential examination of the medications administered, we noted that the patient had received morphine by continuous infusion in both cases, 4 to 6 hours before the acute respiratory decompensation. No other drug had been administered at either of those times. All probable causes were excluded and a meticulous analysis of possible rare causes was performed. The diagnosis of morphine-induced ALI was thus made. If the cause of severe respiratory insufficiency is unclear, a differential diagnosis of morphine-induced ALI should be considered.
References [1] Lusk JA, Maloley PA. Morphine-induced pulmonary edema. Am J Med 1988;84:367-8. [2] Vaeusorn N. Pulmonary edema in acute morphine intoxication. A case report. J Med Assoc Thai 1970;53:894-6. [3] Brimacombe J, Archdeacon J, Newell S, Martin J. Two cases of naloxone-induced pulmonary oedema—the possible use of phentolamine in management. Anaesth Intensive Care 1991;19:578-80.
303 [4] Gould DB. Buprenorphine causes pulmonary edema just like all other mu-opioid narcotics. Upper airway obstruction, negative alveolar pressure. Chest 1995;107:1478-9. [5] Harrington LW. Acute pulmonary edema following use of naloxone: a case study. Crit Care Nurse 1988;8:69-73. [6] Johnson C, Mayer P, Grosz D. Pulmonary edema following naloxone administration in a healthy orthopedic patient. J Clin Anesth 1995;7: 356-7. [7] Schwartz JA, Koenigsberg MD. Naloxone-induced pulmonary edema. Ann Emerg Med 1987;16:1294-6. [8] Sporer KA, Dorn E. Heroin-related noncardiogenic pulmonary edema: a case series. Chest 2001;120:1628-32. [9] Sterrett C, Brownfield J, Korn CS, Hollinger M, Henderson SO. Patterns of presentation in heroin overdose resulting in pulmonary edema. Am J Emerg Med 2003;21:32-4. [10] Taff RH. Pulmonary edema following naloxone administration in a patient without heart disease. Anesthesiology 1983;59:576-7. [11] Ward CF. Pulmonary edema and naloxone [Letter]. J Clin Anesth 1996;8:690. [12] Sporer KA. Acute heroin overdose. Ann Intern Med 1999;130:584-90. [13] Henderson CA, Reynolds JE. Acute pulmonary edema in a young male after intravenous nalmefene. Anesth Analg 1997;84:218-9. [14] Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 2004;351:327-36. [15] Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000;342:1301-8. [16] Kallet RH, Jasmer RM, Pittet JF, et al. Clinical implementation of the ARDS network protocol is associated with reduced hospital mortality compared with historical controls. Crit Care Med 2005;33:925-9. [17] Köninger J, Friess H, Wagner M, Kadmon M, Büchler MW. Technique of pancreas-preserving duodenectomy. Chirurg 2005;76:273-81.
Case report
Morphine-induced acute lung injury Christian Hainer MD (Staff Anesthesiologist)a , Moritz N. Wente MD, MSc (Staff Surgeon)b , Peter J. Hallscheidt MD (Professor)c , Jan Schmidt MD (Professor)b , Eike Martin MD (Professor and Chairman)a , Markus W. Büchler MD (Professor and Chairman)b , Markus A. Weigand MD (Professor)a,⁎ a
Department of Anaesthesiology, University of Heidelberg, D-69120 Heidelberg, Germany Department of Surgery, University of Heidelberg, D-69120 Heidelberg, Germany c Department of Diagnostic Radiology, University of Heidelberg, D-69120 Heidelberg, Germany b
Received 20 December 2006; revised 18 October 2007; accepted 24 October 2007
Keywords: Acute lung injury; Morphine; Postoperative care
Abstract A 38-year-old woman who had familial adenomatous polyposis was admitted to the intensive care unit with an episode of severe sepsis 5 days after undergoing a pancreas-preserving duodenectomy. Laparotomy with removal of an intra-abdominal abscess, followed by closed postoperative continuous lavage for 10 days, was performed. During two courses of planned tracheal extubation, the patient developed an acute lung injury, making a reintubation necessary. In both events, the patient received small doses of continuous morphine before the extubation. Morphine may induce the development of an acute lung injury in patients, whereas the exact pathophysiologic and pharmacologic mechanisms remain unclear. © 2008 Elsevier Inc. All rights reserved.
1. Introduction Morphine is still the most widely used analgesic in the intensive care unit (ICU) worldwide. Although the summary of product characteristics for morphine points out that “noncardiogenic pulmonary edema has been observed in intensive-care patients,” very few reports about this issue can be found in the scientific literature [1,2]. In addition to opioid-induced acute lung injury (ALI), there are a number of publications on the occurrence of pulmonary edema after The first two authors contributed equally to the preparation of the article. ⁎ Corresponding author. Tel.: +49 6221 56 6350; fax: +49 6221 56 5345. E-mail address: [email protected] (M.A. Weigand). 0952-8180/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.jclinane.2007.10.017
heroin intoxication and administration of naloxone and buprenorphine [3-11]. The exact mechanisms of these effects are not yet fully understood; opioid-induced ALI occurring approximately two to 4 hours after drug intake is characterized by dyspnea, significant hypoxia, and bilateral infiltrates [12]. Clinical remission is quickly achieved when the triggering substance is eliminated, with the pathologic radiograph changes receding more slowly than the clinical symptoms [13]. Elimination of the harmful substance is the primary objective in the treatment of opioid-induced ALI. Subsequent treatment will depend on the severity of the hypoxia and should follow treatment protocols as published by the Adult Respiratory Distress (ARDS) Network [14-16].
Morphine-induced acute lung injury
301
2. Case report Five days after undergoing a pancreas-preserving duodenectomy, a 38 year-old woman who had familial adenomatous polyposis (FAP) was admitted to the ICU with severe signs of sepsis [17]. She received empirical therapy with imipenem/cilastatin. Computed abdominal tomography (CT) showed signs of an intra-abdominal abscess. Emergency laparotomy showed biliary ascites with no direct signs of an anastomotic insufficiency, but with signs of a putative former leakage via the anastomosis between the neoduodenum and biliary tract and the pancreas, respectively. After extensive lavage, irrigation-suction drains were placed. Then postoperative closed continuous lavage was administered. The patient required mechanical ventilation with an inspired oxygen concentration (FIO2) of 0.5 (PaO2/FIO2 235) and continuous norepinephrine (0.15 μg/kg body weight per min). Before receiving mechanical ventilation, the patient was sedated with propofol/sufentanil (1.9 μg/kg body weight per hr). The intra-abdominal smear showed Enterobacter faecium and Candida glabrata; therefore, antibiotic therapy was augmented with vancomycin and caspofungin. The values for the infection parameters subsequently improved, and the continuous dose of initially required norepinephrine was then gradually reduced. During daily sedation withdrawal, the patient showed agitated-anxious behavior based on a history of anxiety disorders. On day 5 after the patient's admission to the ICU, the analgesic treatment was switched from sufentanil to morphine (0.1 mg/kg body weight per hr). Three hours later,
Fig. 1 Chest radiograph showing poorly defined ground glass opacities involving the lower lung zones.
Fig. 2 Chest radiograph showing bilateral areas of consolidation involving mainly the regions of the lower lobes.
after a successful spontaneous breathing trial, the patient's trachea was successfully extubated. Approximately one hour after extubation, the patient's oxygen demand increased significantly; she then subjectively experienced increasing dyspnea. Despite noninvasive ventilation with the pressure support ventilation mode (inspiratory pressure support 18 cm H2O, positive end-expiratory pressure of 8 cm H2O, with a terminal FIO2 of 1.0), respiratory insufficiency worsened (Fig. 1). Three hours after extubation, reintubation was required. A transthoracic echocardiogram (TTE; normal biventricular systolic and diastolic function, no regional wall motion abnormalities, no right ventricular enlargement, and no paradoxic septum motion) excluded pulmonary embolism or cardiogenic pulmonary edema (CPE). The subsequent chest radiograph showed cloudiness on both sides (Fig. 2). A bronchoscopy was performed to verify or exclude a potential aspiration. As PaO2 decreased further to 44 mmHg, nitric oxide inhalation at 5 ppm was started. With the patient placed in the prone position so as to induce deep sedation and comfort with the respirator, light analgesia with morphine was replaced by sufentanil/midazolam. After two hours, the pulmonary situation improved to the point that the respiratory parameter values could be reduced (FIO2, 0.5; positive end-expiratory pressure, 10 mbar; positive inspiratory pressure, 25 mbar; respiratory rate, 16 breaths per minute) and the supply of norepinephrine was discontinued. Another chest radiograph showed markedly reduced cloudiness. In the afternoon, a thoracic spiral CT scan showed peribronchial consolidation in both lower lobes; the abdominal CT showed fluid collections leading to relaparotomy. Intraoperatively, two hematomas were lavaged; again, there was no indication of anastomotic insufficiency.
302
Fig. 3 Computed tomography of the chest showing patchy peripheral and bronchial consolidation with patchy ground glass of the right and left lower lobe; in addition, a small left anterior pneumothorax was diagnosed.
The following day, sedation was reduced and pressure support ventilation was restarted. On day 3, the patient was switched again from sufentanil to morphine. After 4 hours, the patient once again reported increased dyspnea, with parallel worsening of blood gas values. Thoracic radiograph showed again an incipient pulmonary edema (Fig. 4). At an FIO2 of 0.7 with the patient in prone position, the sedation was again switched from morphine to sufentanil/midazolam. Complete resolution of the situation was achieved within 6 hours. No change in infection parameters was observed. After an intensive chart review, morphineinduced ALI was now suspected; the patient received no further exposure to that substance. On the next day, an uncomplicated percutaneous dilational tracheotomy was performed. The patient was able to start weaning from ventilation over the next several days. Eight days later, the tracheotomy cannula was removed. The patient was fully stable without the need for oxygen.
C. Hainer et al. from CPE. In some situations, the severity of the hypoxia can assist in distinguishing between ARDS/ALI and CPE. In the early stages of ARDS/ALI, hypoxia is often more pronounced than the radiologic pathology would suggest, whereas the radiologic pathology dominates over hypoxemia in the early stages of CPE. In the present case, the patient exhibited an increase in oxygen demand with a saturation of 88% but only minor pathologic radiologic signs (Fig. 1). The radiograph taken two hours later clearly showed bihilar infiltrates (Fig. 2). A radiograph is not a reliable adjunct for distinguishing between ARDS and CPE. Cardiogenic pulmonary edema could be excluded by TTE, because the prevailing acoustic conditions were very favorable. Both the left and right ventricles showed good function. In the absence of any signs of right ventricular overload and diastolic dysfunction, acute pulmonary edema also could be ruled out. In spite of the patient's poor respiratory situation, a bronchoscopy was performed to rule out aspiration as a causative factor. The bronchial system was largely without pathologic findings, with the exception of a moderate amount of glassy secretion. A thoracic/abdominal CT scan was performed approximately 16 hours after the acute event. Two artifacts were found below the abdominal wall, which were removed surgically three hours later and identified as noninfected hematomas. Thoracic CT scan showed bilateral striated, partly spotty dense areas; the small ventral pneumothorax in the left thoracic cavity was treated by insertion of a chest tube (Fig. 3). The subsequent rapid remission of the clinical situation was remarkable. The radiograph also showed evidence of surprising improvement (Fig. 4). Three
3. Discussion Patients in ICUs are at high risk for drug side effects and interactions. In this report, we present a case of morphineinduced ALI. Adult respiratory distress syndrome and ALI can occur from a wide diversity of associated conditions, with sepsis being the most common cause. Multiple transfusions, severe trauma, lung contusion, and aspiration of gastric acid are also independent risk factors for ARDS and ALI. The clinical syndromes have to be differentiated
Fig. 4 Chest radiograph after second episode of morphineinduced unspecific acute lung injury, with almost complete recovery.
Morphine-induced acute lung injury days after the acute event, a very similar situation arose. Again, morphine had been administered to support the weaning process. This was the situation in which druginduced ALI was first considered as a differential diagnosis. Other possible causes, such as acute bronchial obstruction or negative pressure pulmonary edema, were ruled out by clinical observation. On closer differential examination of the medications administered, we noted that the patient had received morphine by continuous infusion in both cases, 4 to 6 hours before the acute respiratory decompensation. No other drug had been administered at either of those times. All probable causes were excluded and a meticulous analysis of possible rare causes was performed. The diagnosis of morphine-induced ALI was thus made. If the cause of severe respiratory insufficiency is unclear, a differential diagnosis of morphine-induced ALI should be considered.
References [1] Lusk JA, Maloley PA. Morphine-induced pulmonary edema. Am J Med 1988;84:367-8. [2] Vaeusorn N. Pulmonary edema in acute morphine intoxication. A case report. J Med Assoc Thai 1970;53:894-6. [3] Brimacombe J, Archdeacon J, Newell S, Martin J. Two cases of naloxone-induced pulmonary oedema—the possible use of phentolamine in management. Anaesth Intensive Care 1991;19:578-80.
303 [4] Gould DB. Buprenorphine causes pulmonary edema just like all other mu-opioid narcotics. Upper airway obstruction, negative alveolar pressure. Chest 1995;107:1478-9. [5] Harrington LW. Acute pulmonary edema following use of naloxone: a case study. Crit Care Nurse 1988;8:69-73. [6] Johnson C, Mayer P, Grosz D. Pulmonary edema following naloxone administration in a healthy orthopedic patient. J Clin Anesth 1995;7: 356-7. [7] Schwartz JA, Koenigsberg MD. Naloxone-induced pulmonary edema. Ann Emerg Med 1987;16:1294-6. [8] Sporer KA, Dorn E. Heroin-related noncardiogenic pulmonary edema: a case series. Chest 2001;120:1628-32. [9] Sterrett C, Brownfield J, Korn CS, Hollinger M, Henderson SO. Patterns of presentation in heroin overdose resulting in pulmonary edema. Am J Emerg Med 2003;21:32-4. [10] Taff RH. Pulmonary edema following naloxone administration in a patient without heart disease. Anesthesiology 1983;59:576-7. [11] Ward CF. Pulmonary edema and naloxone [Letter]. J Clin Anesth 1996;8:690. [12] Sporer KA. Acute heroin overdose. Ann Intern Med 1999;130:584-90. [13] Henderson CA, Reynolds JE. Acute pulmonary edema in a young male after intravenous nalmefene. Anesth Analg 1997;84:218-9. [14] Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 2004;351:327-36. [15] Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000;342:1301-8. [16] Kallet RH, Jasmer RM, Pittet JF, et al. Clinical implementation of the ARDS network protocol is associated with reduced hospital mortality compared with historical controls. Crit Care Med 2005;33:925-9. [17] Köninger J, Friess H, Wagner M, Kadmon M, Büchler MW. Technique of pancreas-preserving duodenectomy. Chirurg 2005;76:273-81.