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Laparoscopy pathophysiology by ma3en abu 7oseh
Laparoscopy pathophysiology by ma3en abu 7oseh
Laparoscopy pathophysiology by ma3en abu 7oseh
Laparoscopy pathophysiology by ma3en abu 7oseh
Laparoscopy pathophysiology by ma3en abu 7oseh
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Laparoscopy pathophysiology by ma3en abu 7oseh

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  • 1. Laparoscopic Surgery PathophysiologyThe unique feature of endoscopic surgery in the peritoneal cavity is the need to lift theabdominal wall from the abdominal organs. Two methods have been devised forachieving this.7 The first, used by most surgeons, is the induction of apneumoperitoneum. Throughout the early twentieth century intraperitoneal visualizationwas achieved by inflating the abdominal cavity with air, using a sphygmomanometerbulb. 8 The problem with using air insufflation is that nitrogen is poorly soluble in bloodand is slowly absorbed across the peritoneal surfaces. Air pneumoperitoneum wasbelieved to be more painful than nitrous oxide pneumoperitoneum but less painful thancarbon dioxide pneumoperitoneum. Subsequently, carbon dioxide and nitrous oxide wereused for inflating the abdomen. N2O had the advantage of being physiologically inert andrapidly absorbed. It also provided better analgesia for laparoscopy performed under localanesthesia when compared with CO2 or air. 9 Despite initial concerns that N2O would notsuppress combustion, controlled clinical trials have established its safety within theperitoneal cavity. 10 In addition, nitrous oxide has recently been shown to reduce theintraoperative end-tidal CO2 and minute ventilation required to maintain homeostasiswhen compared to CO2 pneumoperitoneum. 10 The effect of N2O on tumor biology andthe development of port site metastasis are unknown. As such, caution should beexercised when performing laparoscopic cancer surgery with this agent. Finally, thesafety of N2O pneumoperitoneum in pregnancy has yet to be elucidated.The physiologic effects of CO2 pneumoperitoneum can be divided into two areas: (1)gas-specific effects and (2) pressure-specific effects (Fig. 13-2). CO2 is rapidly absorbedacross the peritoneal membrane into the circulation. In the circulation, CO 2 creates arespiratory acidosis by the generation of carbonic acid. 11 Body buffers, the largestreserve of which lies in bone, absorb CO2 (up to 120 L) and minimize the developmentof hypercarbia or respiratory acidosis during brief endoscopic procedures. 11 Once thebody buffers are saturated, respiratory acidosis develops rapidly, and the respiratorysystem assumes the burden of keeping up with the absorption of CO2 and its releasefrom these buffers.In patients with normal respiratory function this is not difficult; the anesthesiologistincreases the ventilatory rate or vital capacity on the ventilator. If the respiratory raterequired exceeds 20 breaths per minute, there may be less efficient gas exchange andincreasing hypercarbia. 12 Conversely, if vital capacity is increased substantially, there isa greater opportunity for barotrauma and greater respiratory motion–induced disruptionof the upper abdominal operative field. In some situations it is advisable to evacuate thepneumoperitoneum or reduce the intra-abdominal pressure to allow time for theanesthesiologist to adjust for hypercarbia. 13 While mild respiratory acidosis probably isan insignificant problem, more severe respiratory acidosis leading to cardiac arrhythmiashas been reported. 14 Hypercarbia also causes tachycardia and increased systemicvascular resistance, which elevates blood pressure and increases myocardial oxygendemand. 11,14 Page 1 | s x x
  • 2. The pressure effects of the pneumoperitoneum on cardiovascular physiology also havebeen studied. In the hypovolemic individual, excessive pressure on the inferior venacava and a reverse Trendelenburg position with loss of lower extremity muscle tone maycause decreased venous return and cardiac output. 11,15 This is not seen in thenormovolemic patient. The most common arrhythmia created by laparoscopy isbradycardia. A rapid stretch of the peritoneal membrane often causes a vagovagalresponse with bradycardia and occasionally hypotension. 16 The appropriatemanagement of this event is desufflation of the abdomen, administration of vagolyticagents (e.g., atropine), and adequate volume replacement. 17With the increased intra-abdominal pressure compressing the inferior vena cava, there isdiminished venous return from the lower extremities. This has been well documented inthe patient placed in the reverse Trendelenburg position for upper abdominal operations.Venous engorgement and decreased venous return promote venous thrombosis. 18,19Many series of advanced laparoscopic procedures in which deep venous thrombosis(DVT) prophylaxis was not used demonstrate the frequency of pulmonary embolus. Thisusually is an avoidable complication with the use of sequential compression stockings,subcutaneous heparin, or low-molecular-weight heparin. 20 In short-durationlaparoscopic procedures, such as appendectomy, hernia repair, or cholecystectomy, therisk of DVT may not be sufficient to warrant extensive DVT prophylaxis.The increased pressure of the pneumoperitoneum is transmitted directly across theparalyzed diaphragm to the thoracic cavity, creating increased central venous pressureand increased filling pressures of the right and left sides of the heart. If the intra-abdominal pressures are kept under 20 mm Hg, the cardiac output usually is wellmaintained. 19,20,21 The direct effect of the pneumoperitoneum on increasingintrathoracic pressure increases peak inspiratory pressure, pressure across the chestwall, and also the likelihood of barotrauma. Despite these concerns, disruption of blebsand consequent pneumothoraces are rare after uncomplicated laparoscopic surgery. 21Increased intra-abdominal pressure decreases renal blood flow, glomerular filtrationrate, and urine output. These effects may be mediated by direct pressure on the kidneyand the renal vein. 22,23 The secondary effect of decreased renal blood flow is to increaseplasma renin release, thereby increasing sodium retention. Increased circulatingantidiuretic hormone (ADH) levels also are found during the pneumoperitoneum,increasing free water reabsorption in the distal tubules. 24 Although the effects of thepneumoperitoneum on renal blood flow are immediately reversible, the hormonallymediated changes, such as elevated ADH levels, decrease urine output for up to 1 hourafter the procedure has ended. Intraoperative oliguria is common during laparoscopy,but the urine output is not a reflection of intravascular volume status; intravenous fluidadministration during an uncomplicated laparoscopic procedure should not be linked tourine output. Because fluid losses through the open abdomen are eliminated withlaparoscopy, the need for supplemental fluid during a laparoscopic surgical procedure israre.The hemodynamic and metabolic consequences of pneumoperitoneum are well toleratedby healthy individuals for a prolonged period and by most individuals for at least a shortperiod. Difficulties can occur when a patient with compromised cardiovascular function is Page 2 | s x x
  • 3. subjected to a long laparoscopic procedure. It is during these procedures that alternativeapproaches should be considered or insufflation pressure reduced. Alternative gases thathave been suggested for laparoscopy include the inert gases helium, neon, and argon.These gases are appealing because they cause no metabolic effects, but are poorlysoluble in blood (unlike CO2 and N2O) and are prone to create gas emboli if the gas hasdirect access to the venous system. 19 Gas emboli are rare but serious complications oflaparoscopic surgery. 20,25 They should be suspected if hypotension develops duringinsufflation. Diagnosis may be made by listening (with an esophageal stethoscope) forthe characteristic "mill wheel" murmur. The treatment of gas embolism is to place thepatient in a left lateral decubitus position with the head down to trap the gas in the apexof the right ventricle. 20 A rapidly placed central venous catheter then can be used toaspirate the gas out of the right ventricle.In some situations minimally-invasive abdominal surgery should be performed withoutinsufflation. This has led to the development of an abdominal lift device that can beplaced through a 10- to 12-mm trocar at the umbilicus. 26 These devices have theadvantage of creating little physiologic derangement, but they are bulky and intrusive.The exposure and working room offered by lift devices also are inferior to thoseaccomplished by pneumoperitoneum. Lifting the anterior abdominal wall causes a"pinching in" of the lateral flank walls, displacing the bowel medially and anteriorly intothe operative field. A pneumoperitoneum, with its well-distributed intra-abdominalpressure, provides better exposure. Abdominal lift devices also cause morepostoperative pain, but they do allow the performance of MIS with standard(nonlaparoscopic) surgical instruments.Early it was predicted that the surgical stress response would be significantly lessenedwith laparoscopic surgery, but this is not always the case. Serum cortisol levels afterlaparoscopic operations are often higher than after the equivalent operation performedthrough an open incision. 27 In terms of endocrine balance, the greatest differencebetween open and laparoscopic surgery is the more rapid equilibration of most stress-mediated hormone levels after laparoscopic surgery. Immune suppression also is lessafter laparoscopy than after open surgery. There is a trend toward more rapidnormalization of cytokine levels after a laparoscopic procedure than after the equivalentprocedure performed by celiotomy. 28Transhiatal mobilization of the thoracic esophagus is commonly performed as acomponent of many laparoscopic upper abdominal procedures. Entering the posteriormediastinum transhiatally exposes the thoracic organs to positive insufflation pressureand may result in decreased venous return and a resultant decrease in cardiac output. Ifthere is compromise of the mediastinal pleura with resultant CO2 pneumothorax, thedefect should be enlarged so as to prevent a tension pneumothorax. Page 3 | s x x
  • 4. 7. Smith RS, Fry WR, et al: Gasless laparoscopy and conventional instruments: The next phase of minimally-invasive surgery. Arch Surg 128:1102, 1993. [PMID: 8215870]8. Litynski GS: Highlights in the history of laparoscopy. Frankfurt am main, Germany: Barbara Bernet, Verlag,1996, p 78.9. Hunter JG, Staheli J, et al: Nitrous oxide pneumoperitoneum revisited: Is there a risk of combustion? SurgEndosc 9:501, 1995. [PMID: 7676370]10. Tsereteli Z, Terry ML, et al: Prospective randomized clinical trial comparing nitrous oxide and carbondioxide pneumoperitoneum for laparoscopic surgery. J Am Coll Surg 195:173, 2002. [PMID: 12168963]11. Callery MP, Soper NJ: Physiology of the pneumoperitoneum, in Hunter (ed): Baillières ClinicalGastroenterology: Laparoscopic Surgery. London/Philadelphia: Baillière Tindall, 1993, p 757.12. Ho HS, Gunther RA, et al: Intraperitoneal carbon dioxide insufflation and cardiopulmonary functions. ArchSurg 127:928, 1992. [PMID: 1386506]13. Wittgen CM, Andrus CH, et al: Analysis of the hemodynamic and ventilatory effects of laparoscopiccholecystectomy. Arch Surg 126:997, 1991. [PMID: 1830738]14. Cullen DJ, Eger EI: Cardiovascular effects of carbon dioxide in man. Anesthesiol 41:345, 1974. [PMID:4412334]15. Cunningham AJ, Turner J, et al: Transoesophageal echocardiographic assessment of haemodynamicfunction during laparoscopic cholecystectomy. Br J Anaesth 70:621, 1993. [PMID: 8329253]16. Harris MNE, Plantevin OM, Crowther A, et al: Cardiac arrhythmias during anaesthesia for laparoscopy. BrJ Anaesth 56:1213, 1984. [PMID: 6237663]17. Borten M, Friedman EA: Choice of anaesthesia, in Laparoscopic Complications: Prevention andManagement. Toronto: BC Decker, 1986, p 173.18. Jorgenson JO, Hanel K, Lalak NJ, et al: Thromboembolic complications of laparoscopic cholecystectomy(Letter). Br Med J 306:518, 1993.19. Ho HS, Wolfe BM: The physiology and immunology of endosurgery, in Toouli JG, Gossot D, Hunter JG(eds): Endosurgery. New York/London: Churchill-Livingstone, 1996, p 163.20. Sackier JM, Nibhanupudy B: The pneumoperitoneum-physiology and complications, in Toouli JG, GossotD, Hunter JG (eds): Endosurgery. New York/London: Churchill-Livingstone, 1996, p 155.21. Kashtan J, Green JF, Parsons EQ, et al: Hemodynamic effects of increased abdominal pressure. J Surg Res30:249, 1981. [PMID: 7230773]22. McDougall EM, Monk TG, Wolf JS Jr., et al: The effect of prolonged pneumoperitoneum on renal functionin an animal model. J Am Coll Surg 182:317, 1996. [PMID: 8605555]23. Lindberg F, Bergqvist D, Bjorck M, Rasmussen I: Renal hemodynamics during carbon dioxide Page 4 | s x x
  • 5. pneumoperitoneum: An experimental study in pigs. Surg Endosc 17:480, 2003. [PMID: 12415336]24. Hazebroek EJ, de Vos tot Nederveen Cappel R, Gommers D, et al: Antidiuretic hormone release duringlaparoscopic donor nephrectomy. Arch Surg 137:600, 2002; discussion 605.25. Ostman PL, Pantle-Fisher FH, Fanre EA, et al: Circulatory collapse during laparoscopy. J Clin Anesth2:129, 1990. [PMID: 2140690]26. Alijani A, Cuschieri A: Abdominal wall lift systems in laparoscopic surgery: Gasless and low-pressuresystems. Semin Laparosc Surg 8:53, 2001. [PMID: 11337737]27. Ozawa A, Konishi F, Nagai H, et al: Cytokine and hormonal responses in laparoscopic-assisted colectomyand conventional open colectomy. Surg Today 30:107, 2000. [PMID: 10664330]28. Burpee SE, Kurian M, Murakame Y, et al: The metabolic and immune response to laparoscopic versus openliver resection. Surg Endosc 16:899, 2002. [PMID: 12163951] Source: Schwartzs Principles of Surgerywww.SAWA2006.com Page 5 | s x x

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