Physiology of Pneumoperitoneum and Anaesthesia in Laparoscopic Surgery


Pneumoperitoneum is the essential component for laparoscopic procedures Even though a gasless approach has been described utilizing an intra-abdominal lift, this approach never been documented as better then pneumoperitoneum in healthy patient. There are several characteristics which are considered optimal for this gas. Since the surgical procedure may include electrocautery, the gas which usually are not able to support combustion is essential. Although oxygen and air would not have significant physiological consequences when absorbed, they assistance combustion as well as would have significant deleterious effects with intravascular embolization. Although nitrous oxide might have limited physiological effects when absorbed and it is highly soluble, thereby limiting its effects with intravascular embolism, like air and oxygen, nitrous oxide supports combustion. Although both helium and argon result in little or no change in PaCO2 when compared to CO2 pneumoperitoneum, the amount of gas that must definitely be injected intravenously to cause death is markedly less with these inert agents compared to CO2. Due to the issues with some other gases, CO2 continues to be only agent commonly used during laparoscopic procedures.

The perfect gas for insuflation during laparoscopy must have the next characteristics:

Limited systemic absorption over the peritoneum
Limited systemic results when absorbed.
Rapid removal if absorbed
Not capable of supporting combustion
High solubility in blood
Limited physiological effects with intravascular systemic embolism.

The principle physiological changes during laparoscopy are made clear below:

Changes because of Patient position

Intraperitoneal insuflation of CO2 is conducted with the patient in a 15-200 Trendelenburg position. The patient’s position will be changed to some steep reverse Trendelenburg (rT) position with right lateral tilt to facilitate retraction of the gallbladder fundus and reduce diaphragmatic dysfuction. The patient’s position might have significant effects about the haemodynamic consequences of pneuoperitoneum. In a number of patients undergoing laparoscopic cholecystectomy, use of transesophageal echocardiography (TOE) monitoring, indicates a significant reduction in left ventricular end-diastolic area on assumption of rT position, indicating decreased venous return. Left ventricular ejection fraction has been shown to be maintained throughout in in any other case healthy patients. However, changes in left ventricular loading conditions may have adverse consequences in patients with cardiovascular disease. Trendelenburg position also causes decreased FRC and decreased pulmonary compliance. Reverse trendelenburg posture can also cause decreased LV preload with decreased LVEF.

Mechanical results of pneumoperitoneum

Increased intra abdominal pressure related to pneumoperitoneum may compress venous capacitance vessels causing an initial increase, then asustained decrease in pre-load. Compression of the arterial vasculature increased after-load and could create a marked rise in calculated systemic vascular resistance (SVR). Cardiac index may be significantly reduced, and the magnitude of the effect is proportional to intra-abdominal pressure achieved. In healthy subjects undergoing laparoscopic cholecystectomy, using transoesophageal Doppler indicates that cardiac output is depressed to a maximum of 28% at an insuflation pressure of 15mm Hg but is taken care of at a insuflation pressure of 7mmHg. In an animal model, the threshold IAP which in fact had minimal results on haemodynamic function is 12 mmHg and recommend this pressure limit to avoid cardiovascular compromise during CO2 insuflation.

Summary of Haemodyanamic Changes due to Mechanical pressure of CO2 insuflation

  • Increased systemic vascular resistance (SVR)
  • Increased Mean Arterial pressure (MAP)
  • Minimal alternation in heartbeat (HR)
  • Increased cerebral blood flow (CBF)
  • Increased intracranial pressure (ICP)
  • Decreased renal blood flow (RBF)
  • Decreased portal blood flow
  • Decreased splanchnic blood flow
  • Decreased pulmonary compliance

CO2 absorption and hypercapnia

Significant hypercapnia and acidosis may occur during laparoscopy due to CO2 absorption. Hypercapnia may cause a decrease in myocardial contractility minimizing arrhythmia threshold. The anticipated direct vascular effect of hypercapnia, generating arteriolar dilation and decreased SVR, is modulated by mechanical and neurohumoral responses, including catecholamine release.

Neurohumoral response

Potential mediators of the increased SVR observed during pneumoperitoneum include vasopressin and catecholamines. Hypercapnia and pneumoperitoneum will probably cause stimulation from the sympathetic central nervous system and catecholamine release. Numerous investigators have reported activation of the reninangiotensin system with vasopressin production along with a marked increase in plasma vasopressin immediately after peritoneal insuflation in healthy patients, and the problem of vasopressin release parallels time course ofchanges in SVR. A fourfold rise in plasma rennin and aldosterone concentrations correlating with increases in MAP was observed changes in CI and SVR suggests a potential cause - effect relationship.

In summary, the haemodynamic reaction to peritoneal insuflation has been well described, an depends upon the interaction of factors that include:

  • Patient positioning
  • Peurohumoral response
  • Patient factors including cardiorespiratory status and intravascular volume.

Pre-Operative Evaluation

As with any pre-operative evaluation, the goal is to identify ongoing acute conditions or chronic problems which may affect the plan for anaesthesia. The pre-operative examination should also identify previously undiagnosed conditions, with non-invasive surgical treatments, the pre-operative laboratory evaluation depends more about the patient’s status than on the procedure itself. Because any of these non-invasive procedures carries the potential for blood loss related to vascular damage from a trocar, a haematocrit and type and screen are suggested.

Pre-medication and anaesthetic induction

For non-emergent procedures, the American Society of Anaesthesiologists (ASA) fasting guidelines ought to be followed. In the majority of patients scheduled for non-invasive procedures (laparoscopy or thoracoscopy), some of numerous anaesthetic induction techniques (intravenous and inhalational) are acceptable. In specific circumstances, gastrointestinal (GI) prophylaxis may include oral antacids, motility agents, and H2 antagonists followed by a modified rapid sequences induction with cricoid pressure. The intravascular status and baseline cardiovascular function should be considered when choosing the option of agent and also the route for anaesthetic induction. Intravenous induction having a barbiturate or propofol, using their associated negative inotropic and vasdilatory properties, migh result, in hypotension in patients with altered cardiovascular contractility or hypovolaemia. Such settings, etomidate provides effective anaesthesia without deleterious effects on cardiovascular function. Pre-operative medication may not be required in the older adolescent patient and also the newborn or infant less than 9-12 months old. The decision concerning the utilization of pre-medication is dependent on the physical status of the patient and associated conditions. For the majority of elective or semi-elective procedures, our practice includes inhalation induction using sevoflurane in 100% oxygen, 15-20 minutes after pre-medication with intravenous medazolam.

Airway management

Endotracheal Intubation and controlled mechanical ventilation comprise the accepted anaesthetic technique to slow up the increase in PaCO2 and to avoid ventilatory compromise due to pneumoperitoneum and initial Trendelenburg position. The laryngeal mask airway (LMA) has been used widely during pelvic laparoscopy. Continuous oesophageal pH monitoring and clinical monitoring didn't detect gastro-oesophageal reflux in patients undergoing gynaecological laparoscopy using LMA. However, this evidence can't be extrapolated to upper abdominal laparoscopy, and high intra-abdominal pressures during laparoscopic cholecystectomy could raise the risk of passive regurgitation of gastric contents. Cuffed endotracheal tube placement will minimize the risk of acid aspiration should relux occur.

The choice of neuromuscular blocking drug will depend on the anticipated duration of surgery and also the individual drug side-effect profile. Turnaround of residual neuromuscular blockade with neostigmine has been reported to increase the incidence of post-operative nausea and vomiting (PONV) following laparoscopy in contrast to spontaneous recovery, plus some practitioners avoid its use. However, other investigators have found no impact on the incidence of PONV associated with the use of neostigmine, and specifically in patients undergoing outpatient gynaecological laparoscopy. Using neostigmine and glycopyrrolate didn't increase the incidence or harshness of PONV. Even minor examples of residual neuromuscular blockade can produce distressing symptoms and should be avoided. Therefore, any benefit from omitting neostigmine must be balanced against the risk of inadequate reversal of neuromuscular blockade.


Standard intra-operative monitoring is suitable for all patients undergoing laparoscopic cholecystectomy. Invasive haemodynamic monitoring might be appropriate in ASA III or IV patients to monitor the cardiovascular response to pneumoperitoneum and position changes and to institute therapy. Endo Tracheal CO2 is most commonly used as a non-invasive indicator of PaCO2 in assessing the adequacy of ventilation during laparoscopic procedures. Patients with low forced expiratory and vital capacity volumes, and higher ASA status showing significant increases in PaCO2 during CO2 pulmonary function tests, may predict those patients at risk for growth and development of hypercapnia and acidosis during laparoscopic cholecystectomy. Even in normal patients it would seem prudent to monitor PaCO2 all the time during the procedure to prevent adverse outcome. Persistent refractory hypercapnia or acidosis may need defiation from the pneumoperitoneum,

Intra-operative care

A number of options are for sale to anaesthetic induction, including inhalation or intravenous techniques. Intravenous access is usually secured in the upper extremity if at all possible, since there are the theoretical effect of increased IAP and decreased onset time of medications administered right into a vein in the lower extremity. While standard practice in paediatric anaesthesia includes the use of uncuffed ETTs in youngsters under 6-8 years of age, an excessive leak around an uncuffed ETT may make maintaining minute ventilation during laparoscopy more difficult. As such, tracheal intubation with a cuffed ETT (0.5 cm small compared to that calculated depending on age) withinfiation from the cuff to some minimum occlusive pressure is definitely an acceptable choice to limit difficulties with ventilation using the increase in IAP and it is effects on resistance and compliance. Following endotracheal intubation, a nasogastric tube is passed to decompress the stomach and limit the opportunity of inadvertent damage during trocar placement. For prolonged procedures, a urinary catheter is placed. Monitoring includes standard ASA monitoring.

Maintenance anaesthesia includes a combination of an inhalational agent supplemented with intravenous opioids (fentanyl 3-5mg/kg). While any of the inhalation agents are acceptable, halothane may be problematic if hypercarbia develops. Nitrous oxide is usually avoided because of its potential for exacerbating postoperative nausea and vomiting, its controversial effects on bowel size, as well as the possibility of its diffusion in the blood stream to the peritoneal space. During laparoscopy, it is possible to achieve intraperitoneal concentrations of nitrous oxide which will support combustion. Neuromuscular blockade can be provided by some of a number of non-depolarizing agents in line with the anticipated duration from the procedure. If not administered as part of the pre-medicant, an anticholinergic agent is administered to avoid vagal refiexes throughout the laparoscopic procedure. Due to the possibility of respiratory changes, exhaled tidal volume and PIO are monitored during insuffiation. Alterations in compliance and resistance may necessitate changes in ventilatory parameters to prevent hypercarbia (increasing respiratory rate, increasing PIP) or hypoxaemia (increasing FiO2, application of PEEP, lengthening from the inspiratory time, or use of an inspiratory pause). Whatever the duration of the procedure, minute ventilation may need to be increased by 25-30% to keep nomocarbia. While much attention has been focused on the respiratory effects to CO2 absorption across the peritoneum and also the increased IAP, other aetiologies should be considered if cardiorespiratory compromise occurs during laparoscopy. Especially with upper abdominal procedures (Nissen fundoplication), CO2 can dissect along the mediastinal fascial planes into the thorax, resulting in pneumothorax.

Additionally, there's a possibility of gas embolism. The physiological consequences of gas embolism are related to: (a) gas, (b) volume, (c) rate of entrainment and (d) patient’s haemodynamic and volume status. Because of its solubility in blood, there are generally few consequences with CO2 embolism unless a large quantity is injected. Once the rate of gas entrainment exceeds the lungs’ capacity to excrete it, pulmonary artery pressure rises, leading to right heart failure and dilation with impedance of left ventricular filling related to ventricular interdependence.

Devices to detect gas embolism

  • Aspiration of air from central venous catheter
  • Mill-wheel murmur heard with oesophageal stethoscope
  • Pulmonary artery catheter
  • End-tidal CO2 (variable response with CO2 embolism)
  • End-tidal nitrogen (useful just for air, not CO2 embolism)
  • Pre-cordial Doppler
  • Transoesophageal echocardiography.

The first step in treatment methods are identifying the problem and notifying the surgeon to stop insuffiating in order to release the pneumoperitoneum. Cardiovascular function is based on ventilation with 100% oxygen, discontinuation of inhalation anaesthetic agents, and resuscitation with fiuids and inotropic agents as needed. Several products are available to monitor for gas embolism, with transoesophageal echocardiography being the most sensitive. However, in line with the low incidence of clinically significant gas embolism during non-invasive procedures, our current practice during laparoscopy and thoracoscopy includes standard ASA monitors.

Following completing the procedure, complete evacuation of CO2 is mandatory to limit issues with post-operative pain and nausea/vomiting. Owing to the relatively high incidence of nausea and vomiting following laparoscopic procedures, our practice includes the pre-emptive utilization of a serotonin antagonist such as managed with a multi-modality approach, including acetaminophen, non-steroidal anti-infiammatory agents, opioids, local infiltration of the trocar insertion sites and regional anaesthesia. Our current practice includes the administration of acetaminophen (15mg/kg orally with midazolam pre-medication or 40mg/kg per rectum after the induction of anaesthesia), fentanyl (2-3 mg) and ketorolac (0.5 mg/kg, maximum 30mg) throughout the procedure, and only local infiltration of the trocar insertion sites or regional block having a rectus sheath block or caudal epidural block. In most cases, at completion of the surgical procedure, residual neuromuscular blockade is reversed and the patient’s trachea extubated.

Aetiology of changes of ventilation during laparoscopy

  • Mainstem intubation
  • Endotracheal tube obstruction
  • Pneumothorax
  • Acid aspiration
  • Bronchospasm
  • Atelectasis
  • Mucus plugging
  • Excessive intra-abdominal pressure
  • Decreased FRC from increased IAP / patient
  • positioning
  • Inadvertent gas embolism
  • Decreased cardiac output
  • Hypercarbia from CO2 absorption
  • Anaesthesia machine malfunction

Other Complications

  • Vascular injury
  • Inadvertant extraperitoneal insuffiation
  • Pneumothorax
  • Pneumoperitonium
  • Gas embolism

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