Circulatory and Respiratory Complications of Carbon Dioxide Insufflation

The CO₂ pneumoperitoneum induces hemodynamic, pulmonary, renal, splanchnic and endocrine pathophysiological changes. Most of them are not clinically significant if appropriate anesthetic care is provided. In some cases complications can develop depending on intra-abdominal pressure, the amount of CO₂ absorbed, the circulatory volume of the patient, the ventilation technique used, the underlying pathologic conditions, and the type of anesthesia. Adequate monitoring and correct management is important to prevent the development of complications. There are efficient prevention methods for each type of complication to profit from the benefits of laparoscopic surgery without concerns regarding its safety.

The cardiovascular system is one of the most challenged systems of the human body during laparoscopy. Changes occurring during CO₂ pneumoperitoneum result from two main factors: hypercarbia (and the subsequent acidosis) and increased intra-abdominal pressure.

CO₂ is highly soluble and therefore is very rapidly absorbed from the peritoneal cavity into circulation. Because absorbed CO₂ can only be excreted through the lungs, hypercarbia can only be avoided by a compensatory hyperventilation by increasing the tidal volume of ventilation in anesthetized patients. Hypercarbia can also develop as a result of a highly increased peritoneal absorption of CO₂ and an insufficiently increased exhaustion of CO₂. Absorption of CO₂ is increased particularly during prolonged surgery using high intra-abdominal pressure. Exhaustion of CO₂ is reduced in patients with compromised cardiopulmonary function and restricted CO₂ clearance [1]. Also, the compensatory hyperventilation is impeded by the Trendelenburg position or a high intra-abdominal pressure, which cause a cephalad displacement of the diaphragm (resulting in reduction of lung volumes) and a restriction in diaphragmatic mobility. In these conditions, severe hypercarbia can develop despite aggressive hyperventilation. It should be stressed that intra-abdominal pressure has a major role in the development of hypercarbia since it both increases the absorption and decreases the exhaustion of CO₂.

Hypercarbia and acidosis can cause hemodynamic changes by direct action on the cardiovascular system and by an indirect action through sympathoadrenal stimulation [1, 2]. The direct effect of carbon dioxide and acidosis can lead to decreased cardiac contractility, sensibilization of myocardium to the arrhythmogenic effects of catecholamines and systemic vasodilatation. The centrally mediated, autonomic effects of hypercarbia lead to a widespread sympathetic stimulation resulting in tachycardia and vasoconstriction counteracting the direct vasodilatatory effect.

Increased intra-abdominal pressure during pneumoperitoneum triggers several pathophysiological mechanisms independently of the type of used gas. The most important mechanism of the neurohumoral response of the vasopressin and renin-angiotensin-aldosterone system is the sympathetic stress response [2]including vagal reflexes. The increased intra-abdominal pressure also leads to a mechanical impairment of the venous blood return leading to an increase in venous pressure of the lower extremity while decreasing the cardiac preload. Depending on the extent of above mentioned mechanisms there will be an increase in systemic vascular resistance and pulmonary vascular resistance resulting in an increased afterload. The development of hemodynamic changes depends on the functional reserve of the heart. There may be a decrease in cardiac output and hypotension without an increase in the heart rate.

Cardiovascular changes have been characterized by many clinical studies [3, 4, 5, 6, 7, 8, 27]. Most of these studies reported increased systemic and pulmonary vascular resistance and reduction of cardiac index when laparoscopy was performed at about 15 mm Hg and head up tilt 10°. Joris et al. [3], using invasive monitoring, observed a significant increase in mean arterial pressure (35%) after peritoneal insufflations, along with an increase of systemic vascular resistance (65%) and pulmonary vascular resistance (90%), and a decrease in cardiac index (20%), while the pulmonary capillary wedge pressure and central venous pressure increased. They suggested that the decrease in cardiac index can be partly explained by an increase in systemic vascular resistance.

Using lower insufflation pressures, changes were milder and transient. Three minutes after the onset of pneumoperitoneum at the pressure of 8–12 mm Hg, Branche et al. [7]observed a 25.7% increase in mean arterial pressure, a 49% increase in left ventricular end-systolic wall stress (a measure of left ventricular afterload ) and a 17% decrease in fractional area shortening (a measure of left ventricular function-contractility). All measured variables returned to preinsufflation values after 30 min of pneumoperitoneum and thereafter were no longer significantly affected by postural changes (10° head-up position) or pneumoperitoneum exsufflation.

A further reduction of the insufflation pressure was possible in children. During laparoscopic fundoplication for gastroesophageal reflux performed in the head-up position (10°) and at 5 mm Hg, an increase of 22% in CI was recorded, along with a 21% increase in mean arterial pressure and a 17% increase in heart rate [9]. The results of all these above mentioned studies illustrate the hemodynamic changes depend directly on intra-abdominal pressure.

The pathophysiological cardiovascular changes commonly occur but are well managed intraoperatively. The ‘true’ complications are represented by hypertension, hypotension, arrhythmias, and cardiac arrest.

Hypertensive episodes are dangerous because of their potential risk for hemorrhagic stroke, pulmonary edema and cardiac decompensation. The true incidence of hypertensive episodes is unknown, mainly because of the impact of pharmacological interventions that most of them are very efficient in controlling hypertention. But its incidence seems to be higher at the beginning of insufflations, when the increasing (but still below 10 mm Hg) intra-abdominal pressure increases the venous return by reducing the blood volume in the splanchnic vasculature. This increased preload augments cardiac output and arterial pressure [10, 11]. This situation commonly occurs in patients having sufficient intravascular volume loading, i.e. ∼10 ml/kg prior to the induction of pneumoperitoneum, a loading which is nowadays standard for the prevention of hypotention.

Hypotension is a rare but serious complication occurring in up to 13% of laparoscopies [12]. It occurs mainly when intra-abdominal pressure exceeds 20 mm Hg due to compression of the inferior vena cava. Venous return from the lower half of the body is impeded resulting in a reduction of cardiac output and hypotension. High intrathoracic pressure during intermittent positive pressure ventilation further impairs venous return and cardiac output, particularly if positive end-expiratory pressures are also applied. A vagal response can be involved in some cases. Since the central venous pressure rather reflects the intrathoracic pressure than the venous return, intraoperative invasive monitoring by a pulmonary artery catheter is required in patients with compromised cardiac function in order to ensure the required effective circulating blood volume to avoid hypotension.

The insufflation of gas into the peritoneal cavity can provoke arrhythmias. Their incidence is as high as 14–27% of laparoscopies [13]which is higher than in ‘open’ surgery. There should be a distinction between sinus tachycardia and ventricular extrasystoles which are due to the release of catecholamines and the more life-threatening bradyarrhythmias (sinus bradycardia, nodal rhythm, atrio-ventricular dissociation and asystole) which are due to a vagal-mediated cardiovascular reflex initiated by rapid stretching of the peritoneum at the beginning of peritoneal insufflation [12, 14]. The incidence of arrhythmias is increased in the use of CO₂ compared to other gases. It results from the myocardial irritability induced directly by CO₂. Most arrhythmias are transient and respond to the reduction of intra-abdominal pressure and 100% O₂ hyperventilation [12, 14].

Cardiac arrest has been reported in 2–20 of 100,000 laparoscopies [13]. Although there are no studies directly comparing the incidence of cardiac arrest in laparoscopic and ‘open’ surgery, the above mentioned numbers are slightly increased compared to the anesthetic intraoperative cardiac arrest rate of 10/100,000 calculated for general surgeries between 1979–1988 [15, 16]. Among the causes of cardiac arrest there are two particularly associated to laparoscopy: the profound vasovagal response to rapid peritoneal distension and gas embolism.

Based on the knowledge of the pathophysiological mechanisms of possible complications, some prophylactic actions can be implemented:

Preoperative intravascular loading (10 ml/kg) ensures an adequate cardiac preload; otherwise the intra-abdominal pressure combined with the head-up tilt position may significantly decrease the cardiac index up to 50% [2, 17, 18, 19, 20]. Case reports of cardiovascular collapse occurring in hypovolemic patients during laparoscopy justify the importance of this procedure.

Intermittent pneumatic compression effectively increases venous return and cardiac preload [21].

Invasive hemodynamic monitoring is required for ASA III and IV patients, including a pulmonary artery catheter for central venous pressure, pulmonary artery pressure [17, 22, 23].

Pharmacological therapy of hypertension, hypotension, and arrhythmia should be available.

Slow insufflation is essential to reduce the fatal consequences of gas embolism (in case of accidental intravascular insufflation) but mainly avoids vasovagal reflexes leading to collapse, arrhytmias and cardiac arrest.

Low intra-abdominal pressure is required, although the optimal pressure cannot be defined. Some procedures were feasible at 5–7 mm Hg [25, 26], but the required abdominal distension varies with surgical procedure, anatomical conditions and myorelaxation. The recommendation is to apply the lowest possible pressure level for each particular case.

Extreme positioning is to be avoided, since it may have an influence both on cardiac preload and ventilation [27]. If certain extreme positions are required for a short time during some procedures, all other possible actions have to be taken in order to get over this critical period.

During pneumoperitoneum the diaphragm is shifted upwards and the abdominal part of the chest wall is stiffened resulting a reduction of the total volume of the lungs, a significant decrease up to 35–40% in pulmonary compliance and a marked increase in the maximum resistance of the respiratory system [28, 29, 30, 31]. Although the decrease in functional residual capacity promotes a ventilation-perfusion mismatch and an intrapulmonary shunting which may lead to hypoxemia [32], this occurs rarely in patients with normal preoperative pulmonary function. Without controlled hyperventilation an increase in the end-tidal carbon dioxide pressure by 10 mm Hg develops. This is why the ventilatory pattern needs to be adjusted, and ventilation with large tidal volumes (12–15 ml/kg) to be performed in order to prevent progressive alveolar atelectasis and hypoxemia and to allow CO₂ elimination. Although ventilation with positive end-expiratory pressure significantly improves pulmonary gas exchange [33, 34]and preserves arterial oxygenation during prolonged pneumoperitoneum [35]it should be noted that positive end-expiratory pressure in the presence of elevated intra-abdominal pressure, increases the intrathoracic pressure and produces marked reduction in cardiac output. Therefore, it should be applied cautiously [36, 37, 38, 39]. A modern ventilation technique is the ‘alveolar recruitment strategy’, consisting of manual ventilation to an airway pressure of 40 cm H₂O for 10 breaths over 1 min, followed by usual mechanical ventilation with mild positive end-expiratory pressure (5 cm H₂O). This improves arterial oxygenation intraoperatively during laparoscopy, without clinical cardiovascular compromise or respiratory complications [40]. Since up to 120 liters of CO₂ can be stored in the human body during pneumoperitoneum, a prolonged mechanical ventilation is needed postoperatively in some cases until CO₂ is eliminated completely [41].

Pulmonary complications are represented by hypoxemia, barotrauma, pulmonary edema, and atelectasis. Gas embolism, subcutaneous emphysema, pneumothorax, pneumomediastinum and pneumopericardum are considered distinct complications of laparoscopy and are discussed separately.

Only patients with compromised cardiopulmonary function such as emphysema and chronic obstructive pulmonary disease are at risk for the development of hypoxemia. If appropriate ventilation and oxygen administration are not able to reverse hypoxemia, conversion to open surgery may be required. Most of the patients with normal cardiopulmonary function will surpass these pathophysiological changes without developing hypoxemia or severe hypercapnia. Elevated airway pressures and decreased compliance could be associated with pulmonary barotrauma, which may occur as an immediate pneumothorax. This is more a theoretical assumption cited by some authors [19], but in the literature there are no such case reports of barotrauma due to inadvertent ventilation during laparoscopy. Although there is an important impairment of pulmonary function and gas exchange during laparoscopy, the recovery of pulmonary function is more rapid and the rate of pulmonary sequelae (atelectasis) or complications (pneumonia) is lower than after open surgical procedures, irrespective to the magnitude of the procedures or age of the patient [42, 43, 44, 45].

Clinically apparent carbon dioxide embolism is a rare complication of laparoscopic surgery (0.0014–0.6% of laparoscopies) [46, 47, 48]but it is associated with a high mortality rate of 28% [13].

The major cause leading to gas emboli is the misplacement of the Veress needle directly into a vein or parenchymal organ, but smaller amounts of gas may also enter circulation through an opening in any injured vessel, either in the abdominal wall or at the operative site. Therefore it is not surprising, that 60% of symptomatic cases occur during initial insufflation. There is level I evidence that the Hasson technique for establishing pneumoperitoneum is safer than the Veress needle technique; the incidence of gas embolism reported by a systematic review was 0.001% (7/489,000 cases) for the Veress needle while no such complication occurred in more than 12,000 cases using the Hasson technique [46]. Therefore the latter is recommended to be used instead of the Veress needle in all cases. The risk of symptomatic gas emboli primarily depends on the type of gas and its solubility. Because of their lower solubility compared to CO₂, the other gases including helium and argon, as well as nitrogen, oxygen and air are at increased risk for embolization (table 1). Nitrous oxide is only slightly less soluble than CO₂ and may have an advantage over the other gases if intravenous embolization occurs. However, it can cause combustion, being hazardous both to the patient and personnel [49].

The number of the clinical events and complications is related directly to the type and amount of gas insufflated. Intravascular presence of small amounts of soluble gas like CO₂ probably occurs frequently without having any clinical consequence, whereas large amounts of a soluble gas or smaller amounts of an insoluble gas (air, nitrous oxide) may cause death. When studied with transesophageal echocardiography, 68% of asymptomatic patients have CO₂ bubbling in the right chamber of the heart during laparoscopic cholecystectomy [50]. Transcranial Doppler experiments have shown that CO₂ bubbles may even reach the cerebral circulation [2]. Since CO₂ is soluble in blood, a much larger amount of it must rapidly enter the vascular system before significant embolism can occur. The dose of gas leading to clinical complications or death in bolus or continuous infusion administration only has been assessed for different gases, in animal experiments. The maximum tolerated doses are presented in table 2. On the basis of a study in dogs, the LD₅₀ for a 70-kg human would be 1,750 ml CO₂ or 375 ml air [51]. In another study the magnitude of physiological disturbances caused by CO₂ was 6.5 times less than that of air [52]. These differences were attributed to the high solubility of CO₂, the buffering capacity of blood for CO₂, and the rapid excretion of CO₂ through the lungs.

Clinically, gas embolism can present as profound hypotension, dyspnea, cyanosis and arrhythmias or asystole. A mill-wheel murmur can be auscultated. There is an initial sudden increase in the end-tidal CO₂ concentration, which decreases later due to cardiovascular collapse. If a gas embolism is suspected, a series of measures have to be immediately performed including [53, 54, 55, 56]:

 – Deflation of pneumoperitoneum.

 – Placement of the patient in Durant’s position (left lateral decubitus with head down position) which allows the gas to rise into the apex of the right ventricle and prevents its entry into the pulmonary artery. The Trendelenburg position is also sufficient as it has the same effect.

 – Hyperventilation and administration of 100% oxygen helps rapid CO₂ elimination.

 – Aggressive cardiopulmonary resuscitation and a central venous catheter should be placed to aspirate the gas.

 – Hyperbaric oxygen is less useful than for air embolisms because CO₂ is more soluble and there is a high pressure gradient between the blood and CO₂ bubbles (over 600 mm Hg) which encourages reabsorption. Use of this technique is only justified if the chamber is available within a short period of time and if it is possible to continue reviving the patient during the oxygen therapy session.

Subcutaneous emphysema has been noted in 0.3–3.0% of laparoscopic procedures [46, 57]. Commonly, the gas passes through any disruption of the peritoneum into the subcutaneous tissue and into the retroperitoneal tissue. It is rarely the consequence of inadvertent placement of trocars and direct insufflation into the subcutaneous tissue. It can extend further on larger areas and even to the mediastinum and pleura, thus being the cause of pneumomediastinum and pneumothorax. The reverse situation is also possible, i.e. the extension of a pneumomediastinum into the subcutaneous tissue.

Mild-to-severe, localized or generalized subcutaneous emphysemas generally do not have clinical consequences. But it might point to a concurrent pneumomediastinum or pneumothorax, which may equally be its cause or effect. If there is an involvement of the neck it is also important to monitor the upper airway for obstruction. As the subcutaneous emphysema constitutes an important reservoir of CO₂ into the body, it leads to an increase in end-tidal CO₂ concentrations and therefore increased ventilation is required.

Since the most used gas in laparoscopy is CO₂, the correct terms to define its pathological presence in the otherwise virtual pleural or pericardiac cavities should use the prefix capno- instead of pneumo-. Although capnothorax is more expected to occur during laparoscopy, a pneumothorax is also possible since the peak and plateau airway pressures of ventilation are higher than in open surgery and could favor, for example, the rupture of a congenital bulla.

Most of the cases of capnothorax occur during those laparoscopic procedures performed near the diaphragm (fundoplications, adrenalectomy) and are obviously caused by accidental diaphragmatic injuries [58, 59, 60, 61, 62]. Beside those situations, there are many other possible routes for gas to enter the thoracic cavity during pneumoperitoneum. Postulated sites are via any congenital diaphragmatic defects (e.g. foramen of Morgagni or foramen of Bochdalek) [63, 64], around the esophageal and aortic hiatus and via any procedure that can damage the falciform ligament (e.g. during insertion of a Veress needle). Occasionally, however, pneumothorax may develop as a result of CO₂ dissecting and spreading through retroperitoneum or by the extension of a subcutaneous emphysema up to pleura. There are even reports of subcutaneous emphysema after laparoscopic extraperitoneal inguinal hernia repair, which extended and produced pneumothorax and pneumomediastinum [65, 66, 67, 68, 69, 70].

As mentioned above, the presence of subcutaneous emphysema should always lead to the suspicion of a capnothorax. Since in both cases, subcutaneous emphysema and capnothorax, the end-tidal CO₂ pressure is increased, the presence of the capnothorax is indicated by oxygen desaturation, increased airway pressure and reduced air entry, and should be confirmed by radiography (table 3).

Occurrence of a capnothorax does not usually require placement of a chest drain, since carbon dioxide gas in the pleural cavity is rapidly reabsorbed at the completion of the procedure, allowing the lung to re-expand rapidly [71, 72]. Meanwhile, the use of positive end-expiratory pressure may largely correct the pathophysiological changes (decrease in total lung thorax compliance, increase in airway pressures, increase in CO₂ absorption, increase in PaCO₂ and end-tidal concentration of CO₂) [3]. Only a moderate to severe capnothorax requires the placement of an intercostal chest tube.

A pneumoperitoneum induces important changes in the physiology of the kidneys. The most common result is oliguria [73]. The main reasons for oliguria during laparoscopy include:

 – Direct mechanical compression of renal arteries, veins and parenchyma [74, 75].

 – The vicious circle of reduced renal perfusion → activation of renin-angiotensin-aldosterone system → renal cortical vasoconstriction [76].

 – Increased antidiuretic hormone (ADH, vasopressin) [76, 77].

 – Reduced cardiac output [78].

All of these factors depend on the amount of intra-abdominal pressure and many experimental studies have documented the inverse correlation between intra-abdominal pressure and both renal perfusion and urine output [74, 75, 79]. At 15 mm Hg the cortical renal flow decreases by 28%, medullar renal flow decreases by 31% [80], glomerular filtration rate decreases to 18–31% of normal values [81]and urine output is below 0.5 ml/min. This is a functional (prerenal) acute renal failure, which is generally reversible after 2 h postoperatively [75]. Prolonged renal hypoperfusion carries the risk for acute tubular necrosis and its consequences. Until now, the clinical significance of some urinary markers for the damage of renal tubules, like N-acetyl-beta-D-glucosaminidase, has not been established [24, 81, 82], but some prophylactic actions are available and can easily be taken before acute tubular necrosis occurs. The easiest method for maintaining renal perfusion is the application of a sufficient intravascular volume loading before and during pneumoperitoneum. Low dose dopamine 2 µg/kg/min can prevent renal dysfunction which is commonly associated with long-lasting surgical laparoscopic procedures performed with higher pressures of pneumoperitoneum (∼15 mm Hg) [83]. Urine output is significantly higher when insufflation of gas at body temperature is used as compared with room temperature CO₂ insufflation. Warm insufflation probably causes a local renal vasodilation and may be beneficial to patients with borderline renal function [20]. Esmolol inhibits the release of renin and blunts the pressor response to induction and maintenance of pneumoperitoneum. Therefore, it may protect the kidneys against renal ischemia during laparoscopy [24, 84]. Non-steroidal anti-inflammatory drugs (NSAIDs), widely used for pain management, can cause renal medullary vasoconstriction that may induce acute tubular necrosis if added to the previous vasoconstriction caused by pneumoperitoneum [85, 86]. Therefore, NSAIDs, both the ‘older’ ones and the new selective COX-2 inhibitors (selective inhibitors of cyclo-oxygenase-2 enzyme) should be avoided preoperatively in patients with impaired renal function or renal diseases.

Experimental animal studies in rats and pigs have shown a decrease in splanchnic macro- and microcirculation depending on the amount of intra-abdominal pressure [87, 88, 89]. The immediate consequences of this relative ischemia were an elevation of various hepatic enzymes, including GOT (glutamic oxaloacetic transaminase) and GPT (glutamic pyruvic transaminase), reflecting hepatocytic damage [90], an impaired function of the Kupffer cells [91], a drop in gastric intramucosal pH [92], an increase in bacterial translocation from the gut, and an increased production of oxygen-derived free radicals [93]. These experimental results were obtained using intra-abdominal pressures ranging from 7 to 30 mm Hg. It is not shown that the effects of the pressures used are equivalent to those in humans and animals, since there is a significant disproportion between the volume of their abdominal cavities.

Clinical studies in patients are rare and consist of only small groups of patients. A very frequently cited study [94]assessed the splanchnic circulatory changes during high-pressure CO₂ pneumoperitoneum. An increase of 5 mm Hg, from 10 to 15 mm Hg, of the intra-abdominal pressure resulted in a blood flow decrease by 40–54% to the stomach, by 32% to the jejunum, by 44% to the colon, by 39% to the liver, and by 60% to the peritoneum. Meanwhile, splanchnic blood flow decreased along with operative time, in spite of a constant intra-arterial pressure. But in humans, the consequences of splanchnic hypoperfusion seem to be milder compared to those encountered in animals.

In laparoscopic cholecystectomy performed at the pressure 12 mm Hg, some studies found no changes in gastric mucosal tonometric values and other studies found a non-significant increase of the gastric mucosal pH (pHi) compared to ‘open’ or ‘gasless’ cholecystectomy [95, 96, 97]. Few studies showed increased levels of aminotransferase (alanine aminotransferase, aspartate aminotransferase) and also of alcohol dehydrogenase and glutathione S-transferase but the phenomenon is transient as these enzymes returned to normal values within 1–3 days [98, 99, 100, 101]. These changes are clinically silent in patients with a normal liver function. Even in selected patients of Child-Pugh classes A and B with compensated cirrhosis some laparoscopic procedures (cholecystectomy, appendectomy, splenectomy) seem to be safe, in any case safer than the ‘open’ procedures [102, 103, 104]. Another concern is that free radicals are generated at the end of the laparoscopic procedure, possibly as a result of an ischemia-reperfusion phenomenon induced by the inflation and deflation of the pneumoperitoneum [105]. There are concerns about the possible oncological consequences since substantial experimental evidence exists implicating that both oxygen- and organic-free radical intermediaries are involved in multiple stages of chemical carcinogenesis (e.g. the nitric oxide pathway appears to play a key role in tumor angiogenesis).

Although the increased level of nitric oxide (implicated in the microvascular dysfunction associated with reperfusion) and malondialdehyde (the end product of lipid peroxidation) stands for an increased splanchnic production of free radicals after laparoscopy [97], many studies assessing different markers of oxidative stress including thiobarbituric acid-reactive substances, plasma total antioxidant status, uric acid, superoxide dismutase, catalase, reduced and oxidized glutathione, and glutathione peroxidase, found significantly less global oxidative stress than in open surgery [106]. Obviously, the influence of reperfusion related mechanisms after laparoscopy and the production of free radicals are smaller than the role of total surgical injury during open surgery [107, 108, 109].

The main pathophysiological changes during laparoscopy refer to the cardiovascular system where they translate into a slight increase in the incidence of arrhythmias and cardiac arrest. All other intraoperative hemodynamic alterations can be effectively prevented and controlled. Although there are important pulmonary pathophysiological changes, hypercarbia, hypoxemia and barotrauma rarely occur due to the appropriate ventilation monitoring and techniques. As long as CO₂ remains the most used gas, significant embolism occurs rarely. The use of other gases (helium and argon) that may have advantages over CO₂ regarding the changes in cardiorespiratory and intraperitoneal immunological status is impeded by their greater risk of embolism. Subcutaneous emphysema does not have clinical consequences but a concurrent capnothorax should be excluded. Usually, because of the high solubility of CO₂, capnothorax is asymptomatic and may be treated conservatively. The alteration in splanchnic perfusion, as well as the systemic hemodynamic changes are proportional to the increased intra-abdominal pressure. Maintaining intra-abdominal pressure under 12 mm Hg reduces the incidences of these changes leading to minimal and transient consecutive organ dysfunction and without consequences for the outcome. It is the merit of the anesthesiology team to not let the pathophysiological changes transform into complications, and the surgeon has to be aware that a low insufflation pressure diminishes the pathophysiologic responses and avoids most of the complications.