Laparoscopic surgery, is it painless?

In recent years, laparoscopic surgery has very quickly become one of the most often performed surgeries. It is usually said that it is less traumatic, the patient recovers quickly, the stay in the clinic is reduced and there is no pain.  Everything said and written is true, but... Is it such a painless and safe surgery? Maybe it depends on how good an anesthesiologist you have.  

Some of the main goals of minimally invasive procedures are to reduce postoperative pain by limiting surgical incisions, to limit damage to lung function, to limit drugs used, thereby decreasing ileus and respiratory depression, and to reduce the potential for prolonged wound healing and hospital stay. Since 1987, when the first laparoscopic cholecystectomy was successfully performed in humans, this has become the gold standard in medicine. 

To have a clear idea of pain and the risks of the procedure, we need to be aware of the anatomy, physiology, pathophysiology, mechanisms, and pathways of pain. This article will mainly discuss the pain issue. 

Laparoscopic surgery involves insufflation of a gas (usually carbon dioxide), with a certain pressure in the peritoneal cavity, producing a pneumoperitoneum. This leads to an increase in intra-abdominal pressure (IAP).  This provides the surgeon with good visibility and enough space for surgery. Two body positions are used to provide even better visibility into the abdominal cavity: Trendelenburg or inverted Trendelenburg. The increased intra-abdominal pressure of the pneumoperitoneum, the change in the patient's position, and the effects of carbon dioxide absorption cause changes in physiology, especially in the cardiovascular and respiratory systems. These changes, as well as the direct effects of gas insufflation, can have significant effects on the patient. 

It is important to understand the anatomy and innervation of the peritoneum so that we can understand its pain. The peritoneum is the largest and most complex serous membrane in the body. It is formed by squamous epithelium (mesothelium) and covers the inner walls of the abdomen and abdominal organs. Its function is to protect the abdominal organs and connect them, thus determining their place in the abdominal cavity and preventing them from rubbing during movement. The mesentery, omentum, and peritoneal ligaments originate from the peritoneum. The parietal peritoneum (PP) is innervated by somatic and visceral afferent nerves. It receives sensitive branches from the inferior intercostal nerves and the superior lumbar nerves. A network of unmyelinated and myelinated nerve fibers can be found anywhere in PP. Unmyelinated fibers are thin and terminate just below PP. Myelinated fibers can penetrate the PP to reach the peritoneal cavity, where they lose their myelin sheath and are exposed to somatic and nociceptive stimuli. PP is sensitive to pain, pressure, touch, friction, cutting, and temperature. Harmful stimuli are perceived as localized and sharp pain. The visceral peritoneum (VP) is not innervated, but the submesothelial tissue is innervated by the autonomic nervous system. Unlike PP, the visceral sub mesothelium also receives fibers from the vagus nerve, in addition to the spinal nerves. VP responds primarily to traction and pressure; not for cutting, burning, or electrical stimulation. The painful stimuli of the VP are poorly localized and blunt. Pain in the structure of the foregut (stomach, duodenum, or bile ducts) refers to the epigastric region, pain in the structure of the middle intestine (appendix, jejunum, or ileum) to the periumbilical region, and pain from a source of the hindgut (distal colon or rectum) refers to the lower abdomen or suprapubic region. Peritoneal adhesions can contain nerve endings. The neurotransmitters in this process are acetylcholine, VIP, serotonin, NO, encephalins, CGRP and substance P. Chronic peritoneal pain can be exacerbated by neurogenic inflammation (pancreatitis). 

The rapid creation of the pneumoperitoneum and the stretching of the peritoneum can lead to the rupture of blood vessels, traumatic cohesion of the nerves, and the realization of inflammatory mediators.  Peritoneal inflammation due to CO2 pressure is also the source of pain after laparoscopy. Carbon dioxide gas can irritate the diaphragm and diaphragm nerve, putting pressure and leading to pain. CO2 itself is the most commonly used gas for abdominal insufflation, as it is colorless, non-toxic, non-flammable, and highly soluble. It is easily absorbed by the peritoneum but causes an increase in Paco2. Increased levels of arterial carbon dioxide due to CO2 resorption can lead to stimulation of the sympathetic nervous system. As activity in the sympathetic nervous system increases, catecholamines also increase. Nerve fibers and the nociceptive response become sensitized, and the pain response intensifies. Increased levels of catecholamines have effects on the cardiovascular system such as tachycardia, increased cardiac contractility, and decreased diastolic filling, which can lead to reduced oxygen supply to the myocardium. 

Although this type of surgery has some advantages over laparotomy, pain management remains one of the factors in the foreground. Without effective pain management, recovery is slower and hospitalization is longer. In addition to the pain at the incision site and the placement of the trocars, there is also diffuse abdominal pain. Pain is most effectively controlled by a multimodal, preventive analgesia approach, such as combining opioids with non-opioid analgesics and local anesthetics. Some novel techniques include aerosolizing the local anesthetic agent into the peritoneal cavity during the laparoscopic procedure. Targeting the peritoneum topically makes sense as it has been shown that gas insufflation with increased intra-abdominal pressure results in peritoneal inflammation and neuronal rupture.  

References: 

1. Peritoneal innervation: embryology and functional anatomy, Florian Struller, Frank-Jürgen Weinreich, Philipp Horvath, Marios-Konstantinos Kokkalis, Stefan Beckert, Alfred Königsrainer and Marc A. Reymond; https://doi.org/10.1515/pap-2017-0024 

2. Pain afetr laparoscopy, J. I. Alexander; British Journal of Anaesthesia 1997;79:369-378 

3. Pain management following laparoscopy. Can we do better?  

   Tobias, Joseph D.; Saudi Journal of Anaesthesia 7(1):p 3-4, Jan–Mar 2013. ; DOI: 10.4103/1658-354X.109553