| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
From the Department of Anesthesia, Tufts-New England Medical Center, Tufts University School of Medicine, Boston, Massachusetts, USA.
Address correspondence to: Dr. Jana Hudcova, Department of Anesthesia, Tufts-New England Medical Center, Box 298, 750 Washington St., Boston, Massachusetts 02111, USA. Phone: 617-636-6044; Fax: 617-636-8384; E-mail: jhudcova{at}tufts-nemc.org
 |
Abstract |
|---|
 TOP Abstract IntroductionCaseDiscussionReferences |
|---|
Clinical features: During anesthesia for laparoscopic pheochromocytoma removal we noticed an abrupt, extensive increase of the end-tidal CO2 accompanied by a change of the capnographic CO2 tracing and reversal of the normal arterial-to-end-tidal gradient. These changes consistently disappeared by intermittent deflation of the abdomen and at the end of surgery. A chest x-ray revealed a right-sided loculated pneumothorax with pleural thickening. Peritoneo-thoracic CO2 tracking and pleural scaring with pulmonary adhesions resulting in a unidirectional communication between the pleural space and airways may best explain the chest x-ray and clinical findings.
Conclusion: Severe intraoperative hypercarbia and arterial to end-tidal CO2 gradient reversal represents an intraoperative challenge. The possibility of a direct communication between the pleural space and the bronchial tree should be considered when other etiologies have been excluded. Simple maneuvers such as abdominal de- and re-inflation and analysis of the end-tidal capnographic tracing might aid in the differential diagnosis and management.
|
Introduction |
|---|
|
TOPAbstractIntroductionCaseDiscussionReferences |
|---|
|
Case |
|---|
|
TOPAbstractIntroductionCaseDiscussionReferences |
|---|
A 72 kg, 5' 4'', 65-yr-old woman presented for laparoscopic resection of a right adrenal pheochromocytoma. She had a history of hyperparathyroidism, and never smoked. The preoperative medical preparation consisted of daily prazosin 24 mg and metyrosine 1.5 g po for three weeks.
Following left radial artery catheterization on the day of surgery, a blood gas analysis (ABG) on room air revealed: pH 7.49, PaCO2 42 mmHg, PaO2 94 mmHg, bicarbonate 32 mmol·L–1. In the operating room invasive and non-invasive blood pressure, oxygen saturation (SpO2), and electrocardiographic monitors were attached to the patient. An uneventful induction of general anesthesia was achieved with the administration of lidocaine 40 mg iv, propofol 130 mg, sufentanyl 25 µg and rocuronium 80 mg. Following endotracheal intubation, the lungs were ventilated volume controlled with a tidal volume of 625 mL, a respiratory rate of 8 breaths·min–1 and an of FIO2 0.4. The peak inspiratory pressure (PIP) was 18 cm H2O and the end-tidal carbon dioxide (PETCO2) was 34 mmHg. A right internal jugular central venous line was inserted prior to surgical incision. Anesthesia was maintained with isoflurane in oxygen and air with an FIO2 of 0.45, and a continuous sufentanyl infusion of 0.1 µg·kg–1·hr–1. Neuromuscular block was maintained with intermittent iv boluses of rocuronium guided by train-of-four monitoring. Vasoactive short acting iv medications were prepared and readily available should hemodynamic instability ensue.
Prior to peritoneal CO2 insufflation to a target pressure of 15 mmHg, the PETCO2 was 33 mmHg and an ABG showed a PaCO2 of 35 mmHg. The PIP and the PETCO2 increased to 28 and 38 mmHg respectively. Dense adhesions in the right upper quadrant required extensive surgical adhesiolysis to separate the liver from the diaphragm. No diaphragmatic injury was apparent. Thirty-five minutes into the case, a sudden increase of the PETCO2 was noted on the capnograph (model M1026A, Philips, Boeblingen, Germany) to values greater than 70 mmHg accompanied by a change in the shape of the capnograph tracing. The previous end-expiratory (alveolar) plateau was replaced by a very steep and irregular CO2 pattern, and each expiration differed from the previous one. The PIP increased from 28 to 30 mmHg. The surgeon was notified, and manual hyperventilation was begun with an FIO2 of 1.0. During this episode, the patient was hemodynamically stable, and no desaturation occurred. Chest wall sc emphysema as an indication of extensive CO2 tracking was absent at this time, bilateral ventilation was confirmed by auscultation to exclude the possibility of a pneumothorax, and there was no new heart murmur suggestive of a CO2 embolism. The CO2 absorber was exchanged to exclude absorber exhaustion as a cause of the observation. Rebreathing was excluded by an unrevealing examination of the anesthesia circuit, the in- and expiratory ventilator valves and the expiratory gas sample tubing. The ABG values at this time were not suggestive of a possible malignant hyperthermia episode: pH 7.45, PaCO2 39.3 mmHg, PaO2 219 mmHg and bicarbonate 27.8 mmol·L.
Mechanical ventilation was adjusted by increasing the respiratory rate to 12 breaths·min–1. The capnograph subsequently displayed a question mark in lieu of a numerical PETCO2 value and was replaced by a Datex-Ohmeda gas analyzer (model 525, Ultima, Helsinki, Finland) suspecting monitor malfunction. The new monitor briefly revealed PETCO2 values between 100 to 115 mmHg. No significant inspiratory CO2 was detected. The minute ventilation was re-adjusted, and a positive end-expiratory pressure of 5 cm H2O was added, resulting in an increase of the PIP to 34 cm H2O. Curiously, with each removal of a laparoscopic instrument and subsequent desufflation of the peritoneum, a sharp decline of the PETCO2 and normalization of the capnographic PETCO2 tracing was observed. The Table
summarizes intraoperative PETCO2 and PaCO2 values. We attributed abrupt intraoperative bidirectional hemodynamic fluctuations to tumour manipulation rather than hypercarbia, because of the poor correlation in the timing of their respective occurrence. Sixty minutes following the initial event, hypercarbia resulted in acute respiratory acidosis (pH to 7.27) which improved by adjusting the ventilation (pH 7.31). A chest x-ray at the completion of surgery, following extubation in the operating room, showed a loculated pneumothorax at the right lateral costophrenic angle with pleural thickening. At this time, right shoulder sc emphysema was also detected. A follow-up chest x-ray four hours later demonstrated resolution of both findings, and the patient recovered uneventfully.
|
|
Discussion |
|---|
|
TOPAbstractIntroductionCaseDiscussionReferences |
|---|
We report an unexpected and sudden increase in PETCO2, an associated change of the capnopgraphic PETCO2 waveform, and the reversal of the PaCO2 to PETCO2 gradient during laparoscopic adrenalectomy for pheochromocytoma. During laparoscopy in healthy subjects, the CO2 gradient either remains unchanged or may increase,9,10 with an exaggerated response in the presence of cardiopulmonary disease.11 The differential diagnosis of sudden intraoperative hypercarbia including sc emphysema absorption, pneumothorax, CO2 embolus, malfunction of the ventilator, circuit or capnograph, as well as CO2 absorber exhaustion were systematically ruled out. In retrospect, additional information from an intraoperative chest x-ray may have been helpful. However, this would have been difficult to obtain and interpret in a patient in the semi-lateral position with "bean bag" support. The initial expected positive gradient in our patient was found to be reversed following detection of an abrupt increase of PETCO2, and remained highly negative even after adjustments of the ventilation.
Subcutaneous emphysema and pneumothorax are well-recognized complications of pneumoperitoneum12,13 and extraperitoneal laparoscopic surgery. Both are more common when the procedure is close to the diaphragm,13 as during an adrenalectomy or fundoplication, and sc emphysema may be exacerbated by retroperitoneal CO2 insufflation.10 Carbon dioxide may enter the pleural cavity or sc tissue via congenital or acquired defects in the diaphragm12,13 or via free spread within the retroperitoneal space. Injury to the falciform ligament may also be implicated.13 Extensive adhesiolysis to mobilize the liver in our patient could have caused diaphragmatic as well as falciform ligamental injury. Intraoperatively we did not detect any signs of pneumothorax or sc emphysema, but severe hypercarbia instead. The PIP changed minimally, air entry was bilateral and equal, and the oxygen saturation was maintained.
Carbon dioxide embolization is a possible but rare complication of laparoscopy. The classic presentation includes an abrupt reduction of PETCO2, hypotension, cyanosis, arrhythmia or asystole and possibly a mill wheel murmur.12,13 However, there are reports of CO2 embolization with a modest increase, rather than decrease of the PETCO2.12,13 We did not detect any new cardiac murmur or sudden hemodynamic instability during the procedure.
A direct communication between the peritoneal cavity and the broncho-alveolar tree via thoracic tracking of CO2 as a cause for our observation is supported by the abnormal capnographic waveform, and the sudden reversal of the PaCO2 to PETCO2 gradient. Termination of peritoneal CO2 insufflation should result in a linear decline of PETCO2 over time.14 In our patient however, intermittent abdominal port release and finally removal at the end of surgery resulted in an abrupt decrease of the capnographic PETCO2 values, normalization of the waveform and a positive arterial to end-tidal CO2 gradient. This suggests an unusual ball-valve mechanism for direct CO2 entry into the airways. Pleural thickening and a loculated pneumothorax at the right lateral costophrenic on the postoperative chest x-ray suggest prior pleuro-pulmonary disease with subsequent scarring, which may explain such a mechanism in our patient. We believe that peri-toneothoracic CO2 tracking resulted in sudden unidirectional opening of this valve-like pleural pathology, each time a certain laparoscopic threshold pressure was surpassed. Two reports describe direct CO2 entry from the pleural cavity into the brochial tree during transthoracic endoscopic surgery using CO2 insufflation.15,16 Olsfanger et al.15 reported a capnographic waveform resulting from an intraoperative lung puncture that was very similar to our observation: no distinct expiratory upstroke and plateau phase, and each expiration differed from the previous one (Figure). Although not present during the initial intraoperative exam, a sc emphysema was revealed postoperatively. It may take time for such a finding to develop, and repeated examination may be necessary to detect it. Its presence suggests extensive CO2 tracking and absorption, contributing to the large, unphysiologic positive CO2 gradient from CO2 reabsorption and mobilization at the end of surgery (Table
).
|
In conclusion, this case describes the possibility of a significant intraoperative CO2 gradient reversal in the setting of hypercarbia during laparoscopic surgery when certain anatomical alterations are present. Such an event poses an intraoperative challenge, and is difficult to interpret. Close collaboration with the surgical team facilitates patient management and establishment of a differential diagnosis.
|
Footnotes |
|---|
Accepted for publication October 28, 2005. Revision accepted November 21, 2005.
Competing interests: None declared.
|
References |
|---|
|
TOPAbstractIntroductionCaseDiscussionReferences |
|---|
2 Shankar KB, Moseley H, Kumar Y, Vemula V, Krishnan A. Arterial to end-tidal carbon dioxide tension difference during anaesthesia for tubal ligation. Anaesthesia 1987; 42: 482–6.[Medline]
3 Fletcher R, Veintemilla F. Changes in the arterial to end-tidal PCO2 differences during coronary artery bypass grafting. Acta Anaesthesiol Scand 1989; 33: 656–9.[Medline]
4 Russell GB, Graybeal JM. The arterial to end-tidal carbon dioxide difference in neurosurgical patients during craniotomy. Anesth Analg 1995; 81: 806–10.[Abstract]
5 Wahba RW, Tessler MJ. Misleading end-tidal CO2 tensions. Can J Anaesth 1996; 43: 862–6.
6 Whitesell R, Asiddao C, Gollman D, Jablonski J. Relationship between arterial and peak expired carbon dioxide pressure during anesthesia and factors influencing the difference. Anesth Analg 1981; 60: 508–12.
7 Fletcher R. The arterial – end-tidal CO2 difference during cardiothoracic surgery. J Cardiothorac Anesth 1990; 4: 105–17.[Medline]
8 Wahba RW, Tessler MJ, Beique F, Kleiman SJ. Changes in PCO2 with acute changes in cardiac index. Can J Anaesth 1996; 43: 243–5.
9 Puri GD, Singh H. Ventilatory effects of laparoscopy under general anaesthesia. Br J Anaesth 1992; 68: 211–3.
10 Sprung J, Kinney MO, Warner MA, Bourke DL. Anesthetic aspects of laparoscopic adrenalectomy for pheochromocytoma. Seminars in Anesthesia, Perioperative Medicine, and Pain 2002; 21: 35–45.
11 Kazama T, Ikeda K, Kato T, Kikura M. Carbon dioxide output in laparoscopic cholecystectomy. Br J Anaesth 1996; 76: 530–5.
12 Wahba RW, Tessler MJ, Kleiman SJ. Acute ventilatory complications during laparoscopic upper abdominal surgery. Can J Anaesth 1996; 43: 77–83.
13 Gutt CN, Oniu T, Mehrabi A, et al. Circulatory and respiratory complications of carbon dioxide insufflation. Dig Surg 2004; 21: 95–105.[Medline]
14 Mullet CE, Viale JP, Sagnard PE, et al. Pulmonary CO2 elimination during surgical procedures using intra- or extraperitoneal CO2 insufflation. Anesth Analg 1993; 76: 622–6.
15 Olsfanger D, Jedeikin R, Fredman B, Shachor D. Tracheal anaesthesia for transthoracic endoscopic sympathectomy: an alternative to endobronchial anaesthesia. Br J Anaesth 1995; 74: 141–4.
16 Biles DT, Carroll GJ, Smith MV, Flynn RT. Elevated end-tidal carbon dioxide during thoracoscopy: an unusual cause. Anesthesiology 1994; 80: 953–5.[Medline]
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
