Department of Anaesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Harvard Medical International Associated Institution, Fetscherstrasse 74, D-01307 Dresden, Germany
*Corresponding author. E-mail axel.heller@mailbox.tu-dresden.de
Accepted for publication: August 9, 2003
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Abstract |
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Br J Anaesth 2004; 92: 58790
Keywords: anaesthetic techniques, epidural; complications, atrial heart septum defect; complications, pulmonary hypertension; lung, thoracoscopy
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Introduction |
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Depending on the surgical procedure, perioperative mortality in patients with Eisenmenger syndrome is 425%.3 The underlying reason is loss of control over the direction and flow of intracardiac shunt, with increasing right-to-left shunt reducing systemic oxygen delivery. Balance of systemic vascular resistance (SVR) and PVR is crucial during surgery.3 Factors altering the balance of SVR and PVR include hypercarbia, hypothermia, atelectasis, uncontrolled vasodilation by anaesthetics, hypovolaemia, pain-induced stress, altered intrathoracic pressures by artificial ventilation, and hypoxia. The best anaesthetic technique (regional anaesthesia, general anaesthesia or a combination of both) to control SVR and intracardiac shunt is controversial.3 Epidural analgesia alone or in combination with general anaesthesia can improve postoperative outcome, particularly in patients with other cardiovascular disease.4
We report the procedure and the precautions we took for one-lung ventilation (OLV) in a patient with Eisenmenger syndrome.
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Case report |
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Perioperative procedure
Oral premedication was with midazolam 3.75 mg. Preoperative arterial PO2 breathing air was 8.3 kPa, PCO2 4.01 kPa, pH 7.47, haemoglobin 12.7 g dl1 and haematocrit 0.39. We placed an epidural catheter at the sixth thoracic intervertebral space (loss of resistance technique, test dose lidocaine 1%, 4 ml) and inserted a catheter in the left radial artery and a thermodilution fibreoptic pulmonary artery catheter (Opticath®, Abbott Laboratories, North Chicago, IL, USA) with the tip in the right pulmonary artery. The preoperative mean PAP ranged between 56 and 73 mm Hg. Systemic arterial oxygen saturation (SaO2) and mixed venous oxygen saturation (SvO2) were continuously monitored and ranged between 92 and 95% and 72 and 94%, respectively. I.V. fluid administration increased central venous pressure from 2 to 8 mm Hg (crystalloids 2000 ml and hydroxy ethyl starch 500 ml). Epidural analgesia (ropivacaine 0.3%, 6 ml) had no effect on arterial pressure or heart rate. Norepinephrine (0.14 µg kg1 min1) was infused to maintain SVR (Fig. 1) before induction of general anaesthesia with fentanyl 4 µg kg1, ketamine 2 mg kg1, pancuronium 1 mg and succinylcholine 2 mg kg1. A left-sided 37F double-lumen endobronchial tube (Broncho-CathTM, Mallinckrodt, Athlone, Ireland) was inserted and the correct position was confirmed by bronchoscopy. Anaesthesia was maintained with propofol 48 mg kg1 h1 and intermittent doses of fentanyl (total 1.25 mg). Since epidural analgesia was performed, regional muscle relaxation was assumed and no further neuromuscular block was used.
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The patient was transferred to the intensive care ward and the first 16 h after surgery were uneventful. Significant blood loss from the chest drains occurred on the following day. At first conservative therapy was tried, but re-intubation of the trachea and inhaled nitric oxide had to be started on day 2. Evacuation of a pleural haematoma was done by thoracotomy on the third day after surgery. In total, infusion of packed red blood cells (3300 ml) and treatment of the coagulopathy with fresh frozen plasma (5500 ml), platelets (750 ml), fibrinogen (3 g) and antithrombin III (1500 IU) was necessary. The patients condition stabilized over the next few days and the tracheal tube was removed on day 5. Continuous epidural analgesia with ropivacaine 0.2% 4 ml h1 was maintained from the time of weaning from the ventilator until day 10.
The lung specimen showed medial hypertrophy and intimal cellular proliferation (Heath-Edwards grade III5) in two thirds and grade IIIIV changes in the other third of the pulmonary arteries and arterioles. These changes are characterized by intimal fibrosis with obliteration of arterioles and small arteries (Grade III) and dilatation as well as plexiform lesions (Grade IV). Pulmonary artery changes of grade IIII are reversible, but not those of higher grades.
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Discussion |
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We prescribed a reduced dose of midazolam (3.75 mg) before surgery because of the risk of hypoventilation and hypoxia. In the anaesthetic management of Eisenmenger syndrome maintenance of SVR and PVR is crucial,3 so PAP, SvO2 and central venous pressure were measured continuously. Fluid infusion and norepinephrine were used to maintain SVR and prevent any increase of right-to-left shunt after induction of general anaesthesia with vasodilation caused by propofol and changes of intrathoracic pressure caused by ventilation. Ketamine was chosen to induce general anaesthesia because it has sympathomimetic effects. Anaesthesia was maintained with propofol because it has less effect on hypoxic pulmonary vasoconstriction than volatile anaesthetics.8 It was expected that propofol would cause less intrapulmonary shunt during OLV than volatile anaesthetics would have done. Reduced sympathetic activity by epidural anaesthesia was possible, but only small amounts of local anaesthetics were used before induction of general anaesthesia, and arterial pressure remained stable in this period. Analgesia was successful for 10 days after surgery, showing that the epidural was active. Since norepinephrine can constrict the pulmonary vessels9 we were prepared to give inhaled nitric oxide to control PVR. In addition, excessive hypoxic pulmonary vasoconstriction during OLV with increased right-to-left shunt and decreased arterial oxygenation could be counterbalanced by vasodilation of well-ventilated areas of the lung with nitric oxide. Epoprostenol was available in case the patient was a nitric oxide non-responder. Epoprostenol should only be used as a last resort because platelet aggregation might be severely affected by this prostacyclin analogue. Because of similar effects on platelets we did not consider aerosolized prostacyclin, which is as potent as nitric oxide for reversing pulmonary hypertension after cardiac surgery.10
Despite concerns over the use of neuraxial blockade and sympathetic block, with possible increased right-to-left shunting11 we used an epidural for both intra- and postoperative analgesia. Intraoperative analgesia was with ropivacaine 18 mg. Until weaning from ventilation on day 5, epidural analgesia was sustained with a continuous infusion of ropivacaine 812 mg h1. We wished to achieve analgesia of the surgical site and control circulatory changes (e.g. tachycardia, hypertension) without causing severe sympathetic block, and avoid side-effects of opioid analgesia, such as nausea or sleepiness. Our experience12 and recent meta-analyses indicate better postoperative oxygenation and lower pulmonary infection rates after thoracic epidural analgesia combined with general anaesthesia, particularly in patients with co-existing cardiovascular disease.4
Postoperative haemorrhage occurs in 1.8% of videoscopic procedures.13 A recent case report, published after this procedure, reported death after severe haemorrhage from inadequate endoscopic stapling and suggested that thoracoscopic lung biopsy is inadvisable in patients with pulmonary hypertension.14 The diagnostic value of lung biopsy must be weighed against potential life-threatening haemorrhage.
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Conclusion |
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Acknowledgements |
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References |
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