- Email: [email protected]
Severe Carbon Dioxide Retention During Second Laparoscopic Surgery for Urgent Repair of an Operative Defect from the Preceding Laparoscopic Surgery
Acta Anaesthesiol Taiwan 2008;46(3):124−128
C ASE R EPORT
Severe Carbon Dioxide Retention During Second Laparoscopic Surgery for Urgent Repair of an Operative Defect from the Preceding Laparoscopic Surgery Hsin-Lun Wu, Kwok-Hon Chan, Mei-Yung Tsou, Chien-Kun Ting* Department of Anesthesiology, Taipei Veterans General Hospital, School of Medicine, National Yang-Ming University, Taipei, Taiwan, R.O.C.
Received: Nov 30, 2007 Revised: Jan 24, 2008 Accepted: Jan 29, 2008 KEY WORDS: carbon dioxide; cholecystectomy, laparoscopic; hypercapnia; pneumoperitoneum, artificial
A 61-year-old male patient underwent laparoscopic cholecystectomy on diagnosis of acute cholecystitis. Thirteen hours later, bile leakage was noted and a second laparoscopic surgery was performed to rectify this. Severe hypercapnia and acute respiratory acidosis occurred during the act of CO2 pneumoperitoneum. The accumulated CO2 could not be eliminated effectively in spite of deliberate adjustment of the respiratory parameters. We suspected that abnormally high CO2 absorption, which outweighed the capability of physiologic elimination in the presence of acute peritonitis, was the cause of the severe CO2 retention in the second laparoscopic surgery. The patient remained intubated with mechanical ventilatory support after surgery. Excessive internal CO2 was washed out gradually and the patient was extubated successfully the next morning. Profound inflammatory responses in peritonitis may increase permeability and absorption of CO2. Hypercapnia can occur as the store of CO2 in the tissues is saturated and there is continuous inflow of external CO2. It usually takes several hours to achieve a steady state of CO2 elimination after desufflation of CO2 pneumoperitoneum and mechanical ventilatory support may sometimes be needed. In conclusion, caution should be taken against hypercapnia and respiratory acidosis in patients with peritonitis undergoing laparoscopic surgery because of the likelihood of these events occurring during the procedure.
1. Introduction Hypercapnia and acidosis are two physiological changes in response to carbon dioxide (CO2) pneumoperitoneum during laparoscopic surgery. Inflation
of the abdominal cavity with CO2 may be associated with pulmonary atelectasis, reduced functional residual capacity, increased airway pressure, increased CO2 absorption from the peritoneum and decreased diaphragmatic excursion caused either by positional
*Corresponding author. Department of Anesthesiology, Taipei Veterans General Hospital, No. 201, Section 2, Shih-Pai Road, Taipei 112, Taiwan, R.O.C. E-mail: [email protected] ©2008 Taiwan Society of Anesthesiologists
Severe carbon dioxide retention during re-laparoscopic surgery change or increased intra-abdominal pressure.1 The accompanying cardiovascular changes may include hypertension related to augmentation of preload or increased systemic and pulmonary vascular resistance, hypotension caused by impaired venous return from inferior vena cava compression, arrhythmia due to stress, high plasma catecholamine levels, a vagal-mediated reflex from peritoneal stretch, or increased sympathetic tone.2,3 These respiratory and circulatory perturbations can be tolerated by physiologic adjustment in healthy individuals, but may pose potential problems in patients with impaired cardiopulmonary reserve. We report a patient without any chronic systemic disease who developed severe CO2 retention and respiratory acidosis while undergoing a second laparoscopic surgery for urgent repair of an operative defect from the preceding laparoscopic surgery which took place some 13 hours before. We suspected that abnormally high CO2 absorption due to acute peritonitis in the setting of CO2 laparoscopic surgery was the cause of this phenomenon. The possible mechanisms and pathophysiologic reactions are discussed.
2. Case Report A 61-year-old male presenting with fever, abdominal pain over the right upper quadrant and periumbilical tenderness was scheduled to receive laparoscopic cholecystectomy on diagnosis of acute cholecystitis. Abdominal ultrasound showed a distended gallbladder with thickened walls and containing gallstones with a sludgy deposit. Laparoscopic cholecystectomy was carried out smoothly under general anesthesia with intraoperative surveillance by electrocardiogram, pulse oximetry, noninvasive blood pressure monitoring, end-tidal CO2 (EtCO2), and body temperature. After creation of a pneumoperitoneum by CO2 inflation, the cystic duct and artery were identified, clipped and carefully cut. The gallbladder was dissected from the liver bed and retrieved via the navel portal. Intra-abdominal pressure was kept at ≤ 15 mmHg throughout the procedure and EtCO2 rose gradually from 30 to 38 mmHg. Adjustment of controlled hyperventilation by increasing the respiratory rate and tidal volume was made. After completion of the 3-hour surgery, the patient emerged from anesthesia and was extubated before leaving the operating room. He was then returned to the ward following a 2-hour uneventful stay in the post-anesthesia care unit. However, unbearable abdominal pain that could not be alleviated by analgesics disturbed his sleep at midnight. Physical examination revealed distension of the abdomen with muscle guarding but without rebound pain. Abdominal ultrasound revealed
125
fluid accumulation over the right subhepatic area and along the right paracolic gutter, from which clear bile-like fluid was aspirated. Thus, urgent laparoscopic exploration was arranged under the impression of bile leakage. The patient came to the operating room with a fever of 38.8ºC, tachycardia of 121 beats/minute, blood pressure of 141/90 mmHg and a SpO2 reading of 91%. Arterial and central venous lines were set up for close hemodynamic monitoring before induction of general anesthesia. Laparoscopic surgery was carried out via the old incisions; bile peritonitis and bile leak from the stump fistula were noted. Peritoneal irrigation with normal saline, repair of the common bile duct fistula, and placement of a J-vac drain in Morison’s pouch were performed. During the maintenance of CO2 pneumoperitoneum, abnormally high EtCO2 was progressively generated and serial arterial blood gas (ABG) analyses showed acute respiratory acidosis with insufficient metabolic compensation. The hypercapnia could not be eliminated effectively by adjusting the inspiration to expiration ratio, respiratory rate, tidal volume or positive end expiratory pressure of the mechanical ventilator while the application of CO2 pneumoperitoneum was still under way. The highest EtCO2 value registered was 55 mmHg. The patient was ventilated with 100% O2 and the SpO2 could be maintained at 100%. Lactated Ringer’s solution was given for hydration and mannitol at a loading dose of 0.5 g/kg followed by continuous infusion was administered to achieve sufficient expansion of intravascular volume and adequate urine output. Arterial CO2 partial pressure (PaCO2) had escalated to 71.2 mmHg (Figure 1) during pneumoperitoneum while serum pH fell to 7.189 with bicarbonate (HCO3−) elevation to 27.3 mmol/L. The PaO2 was acceptable at 224.2 mmHg. After surgery, the patient remained intubated for mechanical ventilatory support in the post-anesthesia care unit. Hypoxemia in consequence of collapse of the right lower lobe and increased pulmonary infiltrations bilaterally, as revealed by chest X-ray, occurred in the post-anesthesia care unit. Oxygenation was improved after bouts of respiratory recruitment (to keep peak inspiratory airway pressure of 40 cmH2O for 40 seconds). After the patient awoke from anesthesia, sedation was provided for ease of prolonged mechanical ventilation to eliminate the excessive internal CO2. Serial ABG tests gradually demonstrated milder metabolic acidosis with respiratory compensation. The shift from marked respiratory acidosis intraoperatively to mild metabolic acidosis postoperatively might be due to a renal compensatory response by excretion of excessive HCO3− produced from the previous hypercapnia and decrease of HCO3− reabsorption in response to CO2
126
H.L. Wu et al EtCO2 or PaCO2 (mmHg)
80
1st L.C.
2nd L.S.
60 40
37
38
30
39
37
71
55
59
52
54
55
65
54
32 34
EtCO2
20
PaCO2 0
0.5 1 1.5 Induction Inflation
2 3 0.5 1 Deflation Induction Inflation Time (hr)
2
2.5 3 Deflation
Figure 1 End-tidal CO2 (EtCO2) and arterial CO2 partial pressure (PaCO2) change with time in the patient who received two sequential laparoscopic surgeries. EtCO2 rose after pneumoperitoneum in the first laparoscopic surgery, reached and maintained a plateau under compensatory controlled mechanical hyperventilation. In the second laparoscopic surgery, EtCO2 rose to a much higher extent and was sustained at a plateau where maximal respiratory CO2 disposal capacity had been met. The ongoing absorption of CO2 was reflected in excessively high PaCO2 and an increasing difference between EtCO2 and PaCO2. 1st L.C. = first laparoscopic cholecystectomy; 2nd L.S. = second laparoscopic surgery; Induction = induction of general anesthesia; Inflation = inflation of CO2 pneumoperitoneum; Deflation = deflation of CO2 pneumoperitoneum.
wash-out by controlled hyperventilation. The patient was extubated successfully the next morning.
3. Discussion Laparoscopic cholecystectomy has largely replaced open cholecystectomy because of its minimal invasiveness, quicker recovery, markedly lower tissue trauma, and early discharge from hospital with the proviso that no complications occur during laparoscopic surgery.4 The major factor which causes pathophysiologic changes, principally in hemodynamics and respiration, during laparoscopic surgery is pneumoperitoneum by CO2 inflation. In our case, two sequential laparoscopic surgeries were carried out within a short interval in two different clinical conditions, namely, relatively normal in the first one and morbid in the second because of peritonitis as a consequence of bile leakage. Abnormally high EtCO2 and PaCO2 were noted in the second laparoscopic surgery despite active respiratory adjustment of the controlled hyperventilation. Hypercapnia might result from CO2 washout disproportionate to increased CO2 absorption. CO2 is commonly used for laparoscopic surgery to produce pneumoperitoneum as it is achromatic, incombustible, inexpensive, highly soluble in blood, quickly diffuses into the tissues and has less risk of gas embolism formation.5 In man, the solubility of CO2 is 20 times higher than that of O2. The absorbed CO2 equilibrates gradually with the body’s CO2 store, which saturates the well-perfused tissues first, followed by the medium-perfused compartments, and lastly the slowly-perfused body parts.
Excess of CO2 is removed by alveolar ventilation. Hypercapnia develops if the amount of absorbed CO2 outweighs physiologic equilibrium and elimination. Mild hypercapnia may not produce significant hemodynamic effects whereas moderate to severe hypercapnia of 50−70 mmHg may decrease cardiac output, stroke volume, systemic blood pressure, and serum pH.6,7 Endogenous catecholamines are also released, resulting in increases in heart rate, systemic blood pressure, and pulmonary artery pressure. Fortunately, there was no marked hemodynamic instability in our case in the presence of severe hypercapnia. As to the gaseous input in CO2 laparoscopic surgery, the absorption of CO2 during CO2 pneumoperitoneum is determined by its intrinsic diffusion and solubility properties, the rate of continuous CO2 inflation, the contact surface area of the cavity, and the partial pressure difference across the membranes. In the two laparoscopic surgeries of our patient, the gas flow rate, temperature and humidity of CO2 used for inflation were the same and the intra-abdominal pressure was limited to ≤ 15 mmHg in both operations. The external CO2 supply did not differ. Retention of CO2 from the laparoscopic surgery taking place 13 hours previously might have elevated the baseline CO2 content before the second laparoscopic surgery; however, this was probably not the major cause of severe hypercapnia during the second procedure. The initial ABG analysis in the second operation (which revealed pH of 7.41, PaO2 of 93 mmHg, PaCO2 of 34 mmHg, and HCO3− of 22.1 mmol/L) demonstrated that the patient was able to compensate for general adverse conditions.
Severe carbon dioxide retention during re-laparoscopic surgery Inadvertent tearing of the peritoneum or CO2 mistakenly entering into the retroperitoneal space during laparoscopic surgery may increase CO2 absorption and cause hypercapnia. Retroperitoneal inflation of CO2 causes more CO2 absorption than intraperitoneal inflation8 because of the abundance of vasculature and areolar connective tissue in the retroperitoneal space, and furthermore the lack of boundaries between the peritoneum and retroperitoneal space may also play a part. This was not likely to happen in our case in the second laparoscopic surgery because the ports of entry were the same as in the previous laparoscopic cholecystectomy and there was no evidence of subcutaneous emphysema or pneumomediastinum noted. In the event of peritonitis, the patient’s resting metabolism increases. The resting metabolic rate can be increased by 30% compared with normal basal metabolism in systemic inflammatory response syndrome.9 Increased body metabolism could indeed add more CO2 to the absorbed CO2 from the pneumoperitoneum in laparoscopic surgery, but this physiologic alteration is unlikely to be the major cause of hypercapnia in healthy individuals as the compensatory respiratory effects and cardiovascular reserve can easily overcome this phenomenon. Several studies have examined CO2 elimination. It has been shown that, in normal conditions, about 100−200 mL of CO2 could be expelled per minute, but the amount can be increased by 14−48 mL/min in case of CO2 inflation.6,8,10,11 In an uneventful process of CO2 pneumoperitoneum, increased pulmonary CO2 elimination as reflected by an increase of EtCO2 occurs in the first 8−10 minutes after initiation of CO2 inflation, and can reach a plateau within 15−20 minutes, and then return to baseline level some 10 minutes after cessation of CO2 inflation.11 Under general anesthesia, the minute ventilation would have to increase by 12−21% to maintain eucapnia. At equilibrium, the amount of CO2 absorbed can be assumed as the portion in the increased elimination of CO2. In our case, the EtCO2 in the second surgery did reach a plateau during CO2 pneumoperitoneum but the PaCO2 showed a sustained increase to an exceptionally high level. This may be explained by significant continuous CO2 absorption into tissue storage beyond the maximal CO2 elimination capacity. By exclusion of other possibilities, it seems that excessive absorption of CO2 from the pneumoperitoneum may have been the most likely cause of severe hypercapnia in our patient during the second laparoscopic surgery. Profound inflammatory reactions in peritonitis may increase regional blood flow, cell membrane permeability and, hence, exaggerate the absorption of CO2. The hypercapnia that ensued may have been due to the overwhelming
127
input of exogenous CO2 and slow balance between tissue storage compartments, despite vigorous efforts to eliminate CO2 accumulation. The condition would resolve only after discontinuation of CO2 pneumoperitoneum. Kazama et al10 demonstrated that the regression equation of excess of CO2 output/body surface area post-laparoscopy is best fitted into a two-compartment model. The time constants of the rapid and slow compartments were 8.2 minutes and 990 minutes, respectively. Because up to 120 L of CO2 can be stored in the human body, prolonged mechanical ventilation is sometimes required for complete CO2 elimination.5 In our patient, we excluded other possible causes of severe hypercapnia and acidosis in the second laparoscopic surgery and we speculate that increased CO2 absorption by the inflamed peritoneum was the contributing factor. Treatment strategies for this condition should be directed to sufficient expansion of fluid volume (10 mL/kg), limitation of intra-abdominal pressure (≤ 15 mmHg), intermittent pneumatic compression to augment venous return, administration of diuretics to maintain adequate urine output, and mechanical ventilatory adjustment to effectively eliminate CO2. Specific cardiac drugs of short duration to treat hypertension, hypotension and arrhythmia should be at hand to meet requirements. Ventilator adjustments which can be helpful to pulmonary function and gas exchange include an increase in minute ventilation by modifying the respiratory rate and tidal volume while at the same time maintaining acceptable peak airway pressure, cautiously applying positive end-expiratory pressure, and intermittently performing alveolar recruitment. All these manipulations are proposed to prevent progressive atelectasis, improve oxygenation, and facilitate CO2 elimination. Postoperative mechanical ventilatory support should be contemplated to remove the excessive accumulation of the absorbed CO2. In conclusion, excessive CO2 absorption, severe hypercapnia and acidosis may be encountered in patients with peritonitis undergoing laparoscopic surgery. We have witnessed a patient, free of cardiac or pulmonary disease, undergoing two laparoscopic surgeries in quick succession, who sustained severe hypercapnia and respiratory acidosis during the second operation in the presence of newly developed peritonitis. Fortunately, with close intraoperative monitoring, supportive measures, and postoperative mechanical ventilatory assistance, no adverse outcome occurred. Delayed release of stored CO2 from various tissue compartments after discontinuation of CO2 pneumoperitoneum should be kept in mind and resolved with caution. In carrying out laparoscopic surgery with CO2 pneumoperitoneum in patients with peritonitis, one should
128
H.L. Wu et al
be aware of the likelihood of the occurrence of hypercapnia and acidosis.
References 1.
2.
3.
4. 5.
Leonard IE, Cunningham AJ. Anaesthetic considerations for laparoscopic cholecystectomy. Best Pract Res Clin Anaesthesiol 2002;16:1−20. Gutt CN, Oniu T, Mehrabi A, Schemmer P, Kashfi A, Kraus T, Büchler MB. Circulatory and respiratory complications of carbon dioxide insufflation. Dig Surg 2004;21:95−105. Nguyen NT, Wolfe BM. The physiologic effects of pneumoperitoneum in the morbidly obese. Ann Surg 2005;241: 219−26. Cunningham AJ, Brull SJ. Laparoscopic cholecystectomy: anesthetic implications. Anesth Analg 1993;76:1120−33. Koivusalo AM, Lindgren L. Effects of carbon dioxide pneumoperitoneum for laparoscopic cholecystectomy. Acta Anaesthesiol Scand 2000;44:834−41.
6.
Sharma KC, Brandstetter RD, Brensilver JM, Jung LD. Cardiopulmonary physiology and pathophysiology as a consequence of laparoscopic surgery. Chest 1996;110:810−5. 7. Girardis M, Broi UD, Antonutto G, Pasetto A. The effect of laparoscopic cholecystectomy on cardiovascular function and pulmonary gas exchange. Anesth Analg 1996;83: 134−40. 8. Streich B, Decailliot F, Perney C, Duvaldestin P. Increased carbon dioxide absorption during retroperitoneal laparoscopy. Br J Anaesth 2003;91:793−6. 9. Kreymann G, Grosser S, Buggisch P, Gottschall C, Matthaei S, Greten H. Oxygen consumption and resting metabolic rate in sepsis, sepsis syndrome, and septic shock. Crit Care Med 1993;21:1012−9. 10. Kazama T, Ikeda K, Kato T, Kikura M. Carbon dioxide output in laparoscopic cholecystectomy. Br J Anaesth 1996;6: 530−5. 11. Mullet CE, Viale JP, Sagnard PE, Miellet CC, Ruynat LG, Counioux HC, Motin JP, et al. Pulmonary CO2 elimination during surgical procedures using intra- or extraperitoneal CO2 insufflation. Anesth Analg 1993;76:622−6.
C ASE R EPORT
Severe Carbon Dioxide Retention During Second Laparoscopic Surgery for Urgent Repair of an Operative Defect from the Preceding Laparoscopic Surgery Hsin-Lun Wu, Kwok-Hon Chan, Mei-Yung Tsou, Chien-Kun Ting* Department of Anesthesiology, Taipei Veterans General Hospital, School of Medicine, National Yang-Ming University, Taipei, Taiwan, R.O.C.
Received: Nov 30, 2007 Revised: Jan 24, 2008 Accepted: Jan 29, 2008 KEY WORDS: carbon dioxide; cholecystectomy, laparoscopic; hypercapnia; pneumoperitoneum, artificial
A 61-year-old male patient underwent laparoscopic cholecystectomy on diagnosis of acute cholecystitis. Thirteen hours later, bile leakage was noted and a second laparoscopic surgery was performed to rectify this. Severe hypercapnia and acute respiratory acidosis occurred during the act of CO2 pneumoperitoneum. The accumulated CO2 could not be eliminated effectively in spite of deliberate adjustment of the respiratory parameters. We suspected that abnormally high CO2 absorption, which outweighed the capability of physiologic elimination in the presence of acute peritonitis, was the cause of the severe CO2 retention in the second laparoscopic surgery. The patient remained intubated with mechanical ventilatory support after surgery. Excessive internal CO2 was washed out gradually and the patient was extubated successfully the next morning. Profound inflammatory responses in peritonitis may increase permeability and absorption of CO2. Hypercapnia can occur as the store of CO2 in the tissues is saturated and there is continuous inflow of external CO2. It usually takes several hours to achieve a steady state of CO2 elimination after desufflation of CO2 pneumoperitoneum and mechanical ventilatory support may sometimes be needed. In conclusion, caution should be taken against hypercapnia and respiratory acidosis in patients with peritonitis undergoing laparoscopic surgery because of the likelihood of these events occurring during the procedure.
1. Introduction Hypercapnia and acidosis are two physiological changes in response to carbon dioxide (CO2) pneumoperitoneum during laparoscopic surgery. Inflation
of the abdominal cavity with CO2 may be associated with pulmonary atelectasis, reduced functional residual capacity, increased airway pressure, increased CO2 absorption from the peritoneum and decreased diaphragmatic excursion caused either by positional
*Corresponding author. Department of Anesthesiology, Taipei Veterans General Hospital, No. 201, Section 2, Shih-Pai Road, Taipei 112, Taiwan, R.O.C. E-mail: [email protected] ©2008 Taiwan Society of Anesthesiologists
Severe carbon dioxide retention during re-laparoscopic surgery change or increased intra-abdominal pressure.1 The accompanying cardiovascular changes may include hypertension related to augmentation of preload or increased systemic and pulmonary vascular resistance, hypotension caused by impaired venous return from inferior vena cava compression, arrhythmia due to stress, high plasma catecholamine levels, a vagal-mediated reflex from peritoneal stretch, or increased sympathetic tone.2,3 These respiratory and circulatory perturbations can be tolerated by physiologic adjustment in healthy individuals, but may pose potential problems in patients with impaired cardiopulmonary reserve. We report a patient without any chronic systemic disease who developed severe CO2 retention and respiratory acidosis while undergoing a second laparoscopic surgery for urgent repair of an operative defect from the preceding laparoscopic surgery which took place some 13 hours before. We suspected that abnormally high CO2 absorption due to acute peritonitis in the setting of CO2 laparoscopic surgery was the cause of this phenomenon. The possible mechanisms and pathophysiologic reactions are discussed.
2. Case Report A 61-year-old male presenting with fever, abdominal pain over the right upper quadrant and periumbilical tenderness was scheduled to receive laparoscopic cholecystectomy on diagnosis of acute cholecystitis. Abdominal ultrasound showed a distended gallbladder with thickened walls and containing gallstones with a sludgy deposit. Laparoscopic cholecystectomy was carried out smoothly under general anesthesia with intraoperative surveillance by electrocardiogram, pulse oximetry, noninvasive blood pressure monitoring, end-tidal CO2 (EtCO2), and body temperature. After creation of a pneumoperitoneum by CO2 inflation, the cystic duct and artery were identified, clipped and carefully cut. The gallbladder was dissected from the liver bed and retrieved via the navel portal. Intra-abdominal pressure was kept at ≤ 15 mmHg throughout the procedure and EtCO2 rose gradually from 30 to 38 mmHg. Adjustment of controlled hyperventilation by increasing the respiratory rate and tidal volume was made. After completion of the 3-hour surgery, the patient emerged from anesthesia and was extubated before leaving the operating room. He was then returned to the ward following a 2-hour uneventful stay in the post-anesthesia care unit. However, unbearable abdominal pain that could not be alleviated by analgesics disturbed his sleep at midnight. Physical examination revealed distension of the abdomen with muscle guarding but without rebound pain. Abdominal ultrasound revealed
125
fluid accumulation over the right subhepatic area and along the right paracolic gutter, from which clear bile-like fluid was aspirated. Thus, urgent laparoscopic exploration was arranged under the impression of bile leakage. The patient came to the operating room with a fever of 38.8ºC, tachycardia of 121 beats/minute, blood pressure of 141/90 mmHg and a SpO2 reading of 91%. Arterial and central venous lines were set up for close hemodynamic monitoring before induction of general anesthesia. Laparoscopic surgery was carried out via the old incisions; bile peritonitis and bile leak from the stump fistula were noted. Peritoneal irrigation with normal saline, repair of the common bile duct fistula, and placement of a J-vac drain in Morison’s pouch were performed. During the maintenance of CO2 pneumoperitoneum, abnormally high EtCO2 was progressively generated and serial arterial blood gas (ABG) analyses showed acute respiratory acidosis with insufficient metabolic compensation. The hypercapnia could not be eliminated effectively by adjusting the inspiration to expiration ratio, respiratory rate, tidal volume or positive end expiratory pressure of the mechanical ventilator while the application of CO2 pneumoperitoneum was still under way. The highest EtCO2 value registered was 55 mmHg. The patient was ventilated with 100% O2 and the SpO2 could be maintained at 100%. Lactated Ringer’s solution was given for hydration and mannitol at a loading dose of 0.5 g/kg followed by continuous infusion was administered to achieve sufficient expansion of intravascular volume and adequate urine output. Arterial CO2 partial pressure (PaCO2) had escalated to 71.2 mmHg (Figure 1) during pneumoperitoneum while serum pH fell to 7.189 with bicarbonate (HCO3−) elevation to 27.3 mmol/L. The PaO2 was acceptable at 224.2 mmHg. After surgery, the patient remained intubated for mechanical ventilatory support in the post-anesthesia care unit. Hypoxemia in consequence of collapse of the right lower lobe and increased pulmonary infiltrations bilaterally, as revealed by chest X-ray, occurred in the post-anesthesia care unit. Oxygenation was improved after bouts of respiratory recruitment (to keep peak inspiratory airway pressure of 40 cmH2O for 40 seconds). After the patient awoke from anesthesia, sedation was provided for ease of prolonged mechanical ventilation to eliminate the excessive internal CO2. Serial ABG tests gradually demonstrated milder metabolic acidosis with respiratory compensation. The shift from marked respiratory acidosis intraoperatively to mild metabolic acidosis postoperatively might be due to a renal compensatory response by excretion of excessive HCO3− produced from the previous hypercapnia and decrease of HCO3− reabsorption in response to CO2
126
H.L. Wu et al EtCO2 or PaCO2 (mmHg)
80
1st L.C.
2nd L.S.
60 40
37
38
30
39
37
71
55
59
52
54
55
65
54
32 34
EtCO2
20
PaCO2 0
0.5 1 1.5 Induction Inflation
2 3 0.5 1 Deflation Induction Inflation Time (hr)
2
2.5 3 Deflation
Figure 1 End-tidal CO2 (EtCO2) and arterial CO2 partial pressure (PaCO2) change with time in the patient who received two sequential laparoscopic surgeries. EtCO2 rose after pneumoperitoneum in the first laparoscopic surgery, reached and maintained a plateau under compensatory controlled mechanical hyperventilation. In the second laparoscopic surgery, EtCO2 rose to a much higher extent and was sustained at a plateau where maximal respiratory CO2 disposal capacity had been met. The ongoing absorption of CO2 was reflected in excessively high PaCO2 and an increasing difference between EtCO2 and PaCO2. 1st L.C. = first laparoscopic cholecystectomy; 2nd L.S. = second laparoscopic surgery; Induction = induction of general anesthesia; Inflation = inflation of CO2 pneumoperitoneum; Deflation = deflation of CO2 pneumoperitoneum.
wash-out by controlled hyperventilation. The patient was extubated successfully the next morning.
3. Discussion Laparoscopic cholecystectomy has largely replaced open cholecystectomy because of its minimal invasiveness, quicker recovery, markedly lower tissue trauma, and early discharge from hospital with the proviso that no complications occur during laparoscopic surgery.4 The major factor which causes pathophysiologic changes, principally in hemodynamics and respiration, during laparoscopic surgery is pneumoperitoneum by CO2 inflation. In our case, two sequential laparoscopic surgeries were carried out within a short interval in two different clinical conditions, namely, relatively normal in the first one and morbid in the second because of peritonitis as a consequence of bile leakage. Abnormally high EtCO2 and PaCO2 were noted in the second laparoscopic surgery despite active respiratory adjustment of the controlled hyperventilation. Hypercapnia might result from CO2 washout disproportionate to increased CO2 absorption. CO2 is commonly used for laparoscopic surgery to produce pneumoperitoneum as it is achromatic, incombustible, inexpensive, highly soluble in blood, quickly diffuses into the tissues and has less risk of gas embolism formation.5 In man, the solubility of CO2 is 20 times higher than that of O2. The absorbed CO2 equilibrates gradually with the body’s CO2 store, which saturates the well-perfused tissues first, followed by the medium-perfused compartments, and lastly the slowly-perfused body parts.
Excess of CO2 is removed by alveolar ventilation. Hypercapnia develops if the amount of absorbed CO2 outweighs physiologic equilibrium and elimination. Mild hypercapnia may not produce significant hemodynamic effects whereas moderate to severe hypercapnia of 50−70 mmHg may decrease cardiac output, stroke volume, systemic blood pressure, and serum pH.6,7 Endogenous catecholamines are also released, resulting in increases in heart rate, systemic blood pressure, and pulmonary artery pressure. Fortunately, there was no marked hemodynamic instability in our case in the presence of severe hypercapnia. As to the gaseous input in CO2 laparoscopic surgery, the absorption of CO2 during CO2 pneumoperitoneum is determined by its intrinsic diffusion and solubility properties, the rate of continuous CO2 inflation, the contact surface area of the cavity, and the partial pressure difference across the membranes. In the two laparoscopic surgeries of our patient, the gas flow rate, temperature and humidity of CO2 used for inflation were the same and the intra-abdominal pressure was limited to ≤ 15 mmHg in both operations. The external CO2 supply did not differ. Retention of CO2 from the laparoscopic surgery taking place 13 hours previously might have elevated the baseline CO2 content before the second laparoscopic surgery; however, this was probably not the major cause of severe hypercapnia during the second procedure. The initial ABG analysis in the second operation (which revealed pH of 7.41, PaO2 of 93 mmHg, PaCO2 of 34 mmHg, and HCO3− of 22.1 mmol/L) demonstrated that the patient was able to compensate for general adverse conditions.
Severe carbon dioxide retention during re-laparoscopic surgery Inadvertent tearing of the peritoneum or CO2 mistakenly entering into the retroperitoneal space during laparoscopic surgery may increase CO2 absorption and cause hypercapnia. Retroperitoneal inflation of CO2 causes more CO2 absorption than intraperitoneal inflation8 because of the abundance of vasculature and areolar connective tissue in the retroperitoneal space, and furthermore the lack of boundaries between the peritoneum and retroperitoneal space may also play a part. This was not likely to happen in our case in the second laparoscopic surgery because the ports of entry were the same as in the previous laparoscopic cholecystectomy and there was no evidence of subcutaneous emphysema or pneumomediastinum noted. In the event of peritonitis, the patient’s resting metabolism increases. The resting metabolic rate can be increased by 30% compared with normal basal metabolism in systemic inflammatory response syndrome.9 Increased body metabolism could indeed add more CO2 to the absorbed CO2 from the pneumoperitoneum in laparoscopic surgery, but this physiologic alteration is unlikely to be the major cause of hypercapnia in healthy individuals as the compensatory respiratory effects and cardiovascular reserve can easily overcome this phenomenon. Several studies have examined CO2 elimination. It has been shown that, in normal conditions, about 100−200 mL of CO2 could be expelled per minute, but the amount can be increased by 14−48 mL/min in case of CO2 inflation.6,8,10,11 In an uneventful process of CO2 pneumoperitoneum, increased pulmonary CO2 elimination as reflected by an increase of EtCO2 occurs in the first 8−10 minutes after initiation of CO2 inflation, and can reach a plateau within 15−20 minutes, and then return to baseline level some 10 minutes after cessation of CO2 inflation.11 Under general anesthesia, the minute ventilation would have to increase by 12−21% to maintain eucapnia. At equilibrium, the amount of CO2 absorbed can be assumed as the portion in the increased elimination of CO2. In our case, the EtCO2 in the second surgery did reach a plateau during CO2 pneumoperitoneum but the PaCO2 showed a sustained increase to an exceptionally high level. This may be explained by significant continuous CO2 absorption into tissue storage beyond the maximal CO2 elimination capacity. By exclusion of other possibilities, it seems that excessive absorption of CO2 from the pneumoperitoneum may have been the most likely cause of severe hypercapnia in our patient during the second laparoscopic surgery. Profound inflammatory reactions in peritonitis may increase regional blood flow, cell membrane permeability and, hence, exaggerate the absorption of CO2. The hypercapnia that ensued may have been due to the overwhelming
127
input of exogenous CO2 and slow balance between tissue storage compartments, despite vigorous efforts to eliminate CO2 accumulation. The condition would resolve only after discontinuation of CO2 pneumoperitoneum. Kazama et al10 demonstrated that the regression equation of excess of CO2 output/body surface area post-laparoscopy is best fitted into a two-compartment model. The time constants of the rapid and slow compartments were 8.2 minutes and 990 minutes, respectively. Because up to 120 L of CO2 can be stored in the human body, prolonged mechanical ventilation is sometimes required for complete CO2 elimination.5 In our patient, we excluded other possible causes of severe hypercapnia and acidosis in the second laparoscopic surgery and we speculate that increased CO2 absorption by the inflamed peritoneum was the contributing factor. Treatment strategies for this condition should be directed to sufficient expansion of fluid volume (10 mL/kg), limitation of intra-abdominal pressure (≤ 15 mmHg), intermittent pneumatic compression to augment venous return, administration of diuretics to maintain adequate urine output, and mechanical ventilatory adjustment to effectively eliminate CO2. Specific cardiac drugs of short duration to treat hypertension, hypotension and arrhythmia should be at hand to meet requirements. Ventilator adjustments which can be helpful to pulmonary function and gas exchange include an increase in minute ventilation by modifying the respiratory rate and tidal volume while at the same time maintaining acceptable peak airway pressure, cautiously applying positive end-expiratory pressure, and intermittently performing alveolar recruitment. All these manipulations are proposed to prevent progressive atelectasis, improve oxygenation, and facilitate CO2 elimination. Postoperative mechanical ventilatory support should be contemplated to remove the excessive accumulation of the absorbed CO2. In conclusion, excessive CO2 absorption, severe hypercapnia and acidosis may be encountered in patients with peritonitis undergoing laparoscopic surgery. We have witnessed a patient, free of cardiac or pulmonary disease, undergoing two laparoscopic surgeries in quick succession, who sustained severe hypercapnia and respiratory acidosis during the second operation in the presence of newly developed peritonitis. Fortunately, with close intraoperative monitoring, supportive measures, and postoperative mechanical ventilatory assistance, no adverse outcome occurred. Delayed release of stored CO2 from various tissue compartments after discontinuation of CO2 pneumoperitoneum should be kept in mind and resolved with caution. In carrying out laparoscopic surgery with CO2 pneumoperitoneum in patients with peritonitis, one should
128
H.L. Wu et al
be aware of the likelihood of the occurrence of hypercapnia and acidosis.
References 1.
2.
3.
4. 5.
Leonard IE, Cunningham AJ. Anaesthetic considerations for laparoscopic cholecystectomy. Best Pract Res Clin Anaesthesiol 2002;16:1−20. Gutt CN, Oniu T, Mehrabi A, Schemmer P, Kashfi A, Kraus T, Büchler MB. Circulatory and respiratory complications of carbon dioxide insufflation. Dig Surg 2004;21:95−105. Nguyen NT, Wolfe BM. The physiologic effects of pneumoperitoneum in the morbidly obese. Ann Surg 2005;241: 219−26. Cunningham AJ, Brull SJ. Laparoscopic cholecystectomy: anesthetic implications. Anesth Analg 1993;76:1120−33. Koivusalo AM, Lindgren L. Effects of carbon dioxide pneumoperitoneum for laparoscopic cholecystectomy. Acta Anaesthesiol Scand 2000;44:834−41.
6.
Sharma KC, Brandstetter RD, Brensilver JM, Jung LD. Cardiopulmonary physiology and pathophysiology as a consequence of laparoscopic surgery. Chest 1996;110:810−5. 7. Girardis M, Broi UD, Antonutto G, Pasetto A. The effect of laparoscopic cholecystectomy on cardiovascular function and pulmonary gas exchange. Anesth Analg 1996;83: 134−40. 8. Streich B, Decailliot F, Perney C, Duvaldestin P. Increased carbon dioxide absorption during retroperitoneal laparoscopy. Br J Anaesth 2003;91:793−6. 9. Kreymann G, Grosser S, Buggisch P, Gottschall C, Matthaei S, Greten H. Oxygen consumption and resting metabolic rate in sepsis, sepsis syndrome, and septic shock. Crit Care Med 1993;21:1012−9. 10. Kazama T, Ikeda K, Kato T, Kikura M. Carbon dioxide output in laparoscopic cholecystectomy. Br J Anaesth 1996;6: 530−5. 11. Mullet CE, Viale JP, Sagnard PE, Miellet CC, Ruynat LG, Counioux HC, Motin JP, et al. Pulmonary CO2 elimination during surgical procedures using intra- or extraperitoneal CO2 insufflation. Anesth Analg 1993;76:622−6.