1Department of Anaesthesia, C Floor OPD, Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF, UK. 2Department of Surgical and Anaesthetic Sciences, K Floor, Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF, UK*Corresponding author
Accepted for publication: November 21, 2000.
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Abstract |
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Br J Anaesth 2001: 86; 5869
Keywords: carbon dioxide, hypercapnia; anaesthetic techniques, rectal insufflation; complications, subcutaneous emphysema; complications, hypercapnia; complications, ventilatory failure
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Introduction |
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TEM avoids many of the problems associated with laparotomy, although complications have been reported. The commonest are bleeding, perforation, incontinence and rectal stricture.2 Our case report highlights an unreported, potentially life-threatening complication: hypercapnia and ventilatory failure requiring reventilation in the post-operative period.
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Case report |
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The patients medical history included mild asthma controlled with inhaled beclomethasone two puffs twice a day and a salbutamol inhaler, which he used less than twice a month.
On the occasion of the TEM no pre-medication was prescribed, at the request of the patient. After pre-oxygenation, anaesthesia was induced with fentanyl 0.1 mg, propofol 150 mg and vecuronium 8 mg. The trachea was intubated and anaesthesia maintained with oxygen and nitrous oxide in a ratio of 1:2 with an end-tidal concentration of enflurane of 0.61.2%. During the 2.5 h of surgery, anaesthesia was supplemented with boluses of morphine and vecuronium to a total of 10 and 12 mg respectively. Standard monitoring was applied, including transcutaneous nerve stimulation.
In the operating theatre the patient was placed in the lithotomy position, then approximately 45° of Trendelenburg tilt with 20° of rotation to the patients left side were applied to facilitate the use of the TEM equipment.
Fifty minutes into the procedure, a sudden rise in the end-tidal carbon dioxide concentration (E'CO2) from 4.3 to 6.8 kPa was noted, recorded by a Datex capnograph. This coincided with a rise in peak airway pressure from 17 to 25 cm H2O, despite no changes in tidal volume or patient position. Anaesthesia was considered to be of adequate depth and the degree of neuromuscular block was measured as one palpable twitch in a train-of-four response. The only finding on auscultation of the chest was bilateral expiratory wheeze. The bronchospasm settled after treatment with an i.v. bolus of salbutamol 250 µg with a further 250 µg infused over the following 30 min. Airway pressure returned to 17 cm H2O and the E'CO2 settled at 6.1 kPa.
For approximately 30 min, all recorded variables remained normal, then the E'CO2 began to rise again. On this occasion, chest sounds were normal with no new respiratory signs. Help was sought from a senior anaesthetist. Core temperature remained normal at 36.8°C. Pulse and arterial blood pressure were within normal limits. Minute ventilation was increased from 4.9 to 9.8 litre min1, the respiratory rate from 8 to 14 b.p.m. and the fresh gas flow from 1 to 4 litre min1. The nitrous oxide was replaced by air, as there was a suspicion that there may have been an undetected pneumothorax. The enflurane was increased and the table tilt reduced to 10°. Despite these measures, the E'CO2 rose to a maximum of 13 kPa during the next 30 min. Oxygen saturation was unchanged at approximately 97%, airway pressure remained less than 20 cm H2O, breath sounds were still unchanged and the patients temperature remained normal. The E'CO2 returned to 6.1 kPa after 30 min as insufflation was progressively reduced and surgery ceased. Ventilation proceeded on oxygen and enflurane. Residual neuromuscular block was antagonized with neostigmine 2.5 mg and glycopyrrolate 0.5 mg, with full recovery of the train-of-four response.
The patient began to breathe spontaneously and rejected the tracheal tube. He was extubated 15 min after the discontinuation of anaesthesia with an E'CO2 of 4.9 kPa, blood pressure 124/56 mm Hg and heart rate 84 b.p.m., and transferred to the recovery area.
On arrival in the recovery area, the patient demonstrated activity equivalent to a Glasgow coma score of 11 (3 for eyes, 6 for movement and 2 for verbal). However, over the next 20 min his level of consciousness deteriorated. The medical staff in the recovery room administered a small dose of doxapram (20 mg) and naloxone 0.4 mg, with no response. On examination, the patient was unresponsive to painful stimuli, haemodynamic parameters were normal, no blood loss was recorded and he was breathing normally at the rate of 1620 b.p.m. The only abnormal finding on initial examination of the chest was left-sided surgical emphysema, and a provisional diagnosis of a pneumothorax was made. Arterial blood gases were analysed and a chest x-ray was taken. Further examination of the patient revealed extensive surgical emphysema across the anterior abdominal wall, both loins, both groins and the left thigh. The chest x-ray confirmed the subcutaneous emphysema. However, there were no signs of a pneumothorax or other abnormal findings. Arterial blood gases with an FIO2 of 0.6, administered by face mask, were pH 6.97, PCO2 16.8 kPa, PO2 32.7 kPa, HCO3 29 mmol litre1, base excess 6.1. In view of the high PCO2 and the altered level of consciousness, the patient was reintubated and ventilated. Propofol 50 mg and succinylcholine 75 mg were used to facilitate intubation and the patient was transferred to the intensive therapy unit (ITU).
No further sedation was given and hourly arterial blood gases were taken. Three hours after arrival on the ITU the patient was fully conscious, with a PaCO2 of 5.4 kPa, and was extubated. One hour later, with no alteration in his level of consciousness, breathing through a Hudson mask approximately 40% oxygen with a respiratory rate of 14 b.p.m., arterial blood gas analysis was pH 7.38, PCO2 5.1 kPa, PO2 13.0 kPa, HCO3 22.5 mmol litre1 and base excess 1.7. The patient returned to the ward the next day and the remainder of his stay in hospital was uneventful.
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Discussion |
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The need for increased minute ventilation to maintain normocapnia during laparoscopic surgery is well known. Minute ventilation increases of 30%3 and 25%4 have been reported as necessary to maintain normocapnia. No clear recommendations for TEM are available, and the dangers of excessive absorption of carbon dioxide are not appreciated.
TEM is a technique practised in a small number of surgical centres. The anticipated problems include patient positioning and the possibility of prolonged surgery. Those not anticipated are the development of extensive subcutaneous emphysema and the hypercapnia resulting from rectal insufflation with carbon dioxide.
Post-operative hypercapnia resulting from a similar mechanism has been described after renal laparoscopic surgery.5 The duration of insufflation, the extraperitoneal approach, the development of subcutaneous emphysema and the extent of the dissection have been shown to be important determinants of the resultant carbon dioxide absorption.
Gas under tension can track along surgically opened tissue planes to produce collections of extraperitoneal gas,6 and we feel this is the likely origin of the subcutaneous emphysema. A flow of carbon dioxide during insufflation of up to 6 litres min1 has been recommended to maintain intrarectal pressure between 12 and 15 mm Hg.2 We suggest that insufflation flow and intrarectal pressure be monitored continually.
The carbon dioxide eliminated after insufflation is a combination of the carbon dioxide produced and that absorbed from dilated visci and surgical emphysema. The Trendelenburg/lithotomy position and the tracking of carbon dioxide to the loins, groins and thighs (areas not easily accessible to the anaesthetist interoperatively) hindered the detection of surgical emphysema in this patient. We suggest that, if unexpectedly high levels of E'CO2 or PaCO2 are detected during or after procedures involving carbon dioxide insufflation, a detailed examination of the patient should be made to detect unusual sites of surgical emphysema.
In the recovery room this patients arterial carbon dioxide concentration continued to rise from the stores contained in his surgical emphysema. This quantity of carbon dioxide eventually overwhelmed his capacity to excrete it. Blair showed that the insufflation of carbon dioxide into the subcutaneous fat of the anterior abdominal wall of anaesthetized juvenile pigs with a fixed minute ventilation causes an increase in arterial carbon dioxide and a decreased pH that may persist for a prolonged period.6 He suggested that patients with similar problems should have repeated measurements of arterial carbon dioxide and remain in the recovery room for prolonged observation.
Our case highlights a potentially life-threatening complication produced by a mechanism similar to Blairs model. This is the first time that this has been reported in a patient undergoing TEM with rectal carbon dioxide insufflation. The dangers of absorbed carbon dioxide may be overcome by adjustments in ventilation interoperatively, but present as delayed and potentially life-threatening hypercapnia in the early post-operative period. We conclude that a patient with arterial hypercapnia or subcutaneous emphysema after the use of carbon dioxide as an insufflating gas should be observed for a prolonged period in the recovery room, with regular arterial carbon dioxide analysis to allow early intervention should ventilatory failure occur.
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References |
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