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Laparoscopic Surgery Pathophysiology


The unique feature of endoscopic surgery in the peritoneal cavity is the need to lift the
abdominal wall from the abdominal organs. Two methods have been devised for
achieving this.7 The first, used by most surgeons, is the induction of a
pneumoperitoneum. Throughout the early twentieth century intraperitoneal visualization
was achieved by inflating the abdominal cavity with air, using a sphygmomanometer
bulb. 8 The problem with using air insufflation is that nitrogen is poorly soluble in blood
and is slowly absorbed across the peritoneal surfaces. Air pneumoperitoneum was
believed to be more painful than nitrous oxide pneumoperitoneum but less painful than
carbon dioxide pneumoperitoneum. Subsequently, carbon dioxide and nitrous oxide were
used for inflating the abdomen. N2O had the advantage of being physiologically inert and
rapidly absorbed. It also provided better analgesia for laparoscopy performed under local
anesthesia when compared with CO2 or air. 9 Despite initial concerns that N2O would not
suppress combustion, controlled clinical trials have established its safety within the
peritoneal cavity. 10 In addition, nitrous oxide has recently been shown to reduce the
intraoperative end-tidal CO2 and minute ventilation required to maintain homeostasis
when compared to CO2 pneumoperitoneum. 10 The effect of N2O on tumor biology and
the development of port site metastasis are unknown. As such, caution should be
exercised when performing laparoscopic cancer surgery with this agent. Finally, the
safety 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 absorbed
across the peritoneal membrane into the circulation. In the circulation, CO 2 creates a
respiratory acidosis by the generation of carbonic acid. 11 Body buffers, the largest
reserve of which lies in bone, absorb CO2 (up to 120 L) and minimize the development
of hypercarbia or respiratory acidosis during brief endoscopic procedures. 11 Once the
body buffers are saturated, respiratory acidosis develops rapidly, and the respiratory
system assumes the burden of keeping up with the absorption of CO2 and its release
from these buffers.

In patients with normal respiratory function this is not difficult; the anesthesiologist
increases the ventilatory rate or vital capacity on the ventilator. If the respiratory rate
required exceeds 20 breaths per minute, there may be less efficient gas exchange and
increasing hypercarbia. 12 Conversely, if vital capacity is increased substantially, there is
a greater opportunity for barotrauma and greater respiratory motion–induced disruption
of the upper abdominal operative field. In some situations it is advisable to evacuate the
pneumoperitoneum or reduce the intra-abdominal pressure to allow time for the
anesthesiologist to adjust for hypercarbia. 13 While mild respiratory acidosis probably is
an insignificant problem, more severe respiratory acidosis leading to cardiac arrhythmias
has been reported. 14 Hypercarbia also causes tachycardia and increased systemic
vascular resistance, which elevates blood pressure and increases myocardial oxygen
demand. 11,14


                                                                              Page 1 |   s   x x
The pressure effects of the pneumoperitoneum on cardiovascular physiology also have
been studied. In the hypovolemic individual, excessive pressure on the inferior vena
cava and a reverse Trendelenburg position with loss of lower extremity muscle tone may
cause decreased venous return and cardiac output. 11,15 This is not seen in the
normovolemic patient. The most common arrhythmia created by laparoscopy is
bradycardia. A rapid stretch of the peritoneal membrane often causes a vagovagal
response with bradycardia and occasionally hypotension. 16 The appropriate
management of this event is desufflation of the abdomen, administration of vagolytic
agents (e.g., atropine), and adequate volume replacement. 17

With the increased intra-abdominal pressure compressing the inferior vena cava, there is
diminished venous return from the lower extremities. This has been well documented in
the patient placed in the reverse Trendelenburg position for upper abdominal operations.
Venous engorgement and decreased venous return promote venous thrombosis. 18,19
Many series of advanced laparoscopic procedures in which deep venous thrombosis
(DVT) prophylaxis was not used demonstrate the frequency of pulmonary embolus. This
usually is an avoidable complication with the use of sequential compression stockings,
subcutaneous heparin, or low-molecular-weight heparin. 20 In short-duration
laparoscopic procedures, such as appendectomy, hernia repair, or cholecystectomy, the
risk of DVT may not be sufficient to warrant extensive DVT prophylaxis.

The increased pressure of the pneumoperitoneum is transmitted directly across the
paralyzed diaphragm to the thoracic cavity, creating increased central venous pressure
and 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 well
maintained. 19,20,21 The direct effect of the pneumoperitoneum on increasing
intrathoracic pressure increases peak inspiratory pressure, pressure across the chest
wall, and also the likelihood of barotrauma. Despite these concerns, disruption of blebs
and consequent pneumothoraces are rare after uncomplicated laparoscopic surgery. 21

Increased intra-abdominal pressure decreases renal blood flow, glomerular filtration
rate, and urine output. These effects may be mediated by direct pressure on the kidney
and the renal vein. 22,23 The secondary effect of decreased renal blood flow is to increase
plasma renin release, thereby increasing sodium retention. Increased circulating
antidiuretic hormone (ADH) levels also are found during the pneumoperitoneum,
increasing free water reabsorption in the distal tubules. 24 Although the effects of the
pneumoperitoneum on renal blood flow are immediately reversible, the hormonally
mediated changes, such as elevated ADH levels, decrease urine output for up to 1 hour
after the procedure has ended. Intraoperative oliguria is common during laparoscopy,
but the urine output is not a reflection of intravascular volume status; intravenous fluid
administration during an uncomplicated laparoscopic procedure should not be linked to
urine output. Because fluid losses through the open abdomen are eliminated with
laparoscopy, the need for supplemental fluid during a laparoscopic surgical procedure is
rare.

The hemodynamic and metabolic consequences of pneumoperitoneum are well tolerated
by healthy individuals for a prolonged period and by most individuals for at least a short
period. Difficulties can occur when a patient with compromised cardiovascular function is
                                                                            Page 2 |   s   x x
subjected to a long laparoscopic procedure. It is during these procedures that alternative
approaches should be considered or insufflation pressure reduced. Alternative gases that
have been suggested for laparoscopy include the inert gases helium, neon, and argon.
These gases are appealing because they cause no metabolic effects, but are poorly
soluble in blood (unlike CO2 and N2O) and are prone to create gas emboli if the gas has
direct access to the venous system. 19 Gas emboli are rare but serious complications of
laparoscopic surgery. 20,25 They should be suspected if hypotension develops during
insufflation. Diagnosis may be made by listening (with an esophageal stethoscope) for
the characteristic "mill wheel" murmur. The treatment of gas embolism is to place the
patient in a left lateral decubitus position with the head down to trap the gas in the apex
of the right ventricle. 20 A rapidly placed central venous catheter then can be used to
aspirate the gas out of the right ventricle.

In some situations minimally-invasive abdominal surgery should be performed without
insufflation. This has led to the development of an abdominal lift device that can be
placed through a 10- to 12-mm trocar at the umbilicus. 26 These devices have the
advantage of creating little physiologic derangement, but they are bulky and intrusive.
The exposure and working room offered by lift devices also are inferior to those
accomplished by pneumoperitoneum. Lifting the anterior abdominal wall causes a
"pinching in" of the lateral flank walls, displacing the bowel medially and anteriorly into
the operative field. A pneumoperitoneum, with its well-distributed intra-abdominal
pressure, provides better exposure. Abdominal lift devices also cause more
postoperative 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 lessened
with laparoscopic surgery, but this is not always the case. Serum cortisol levels after
laparoscopic operations are often higher than after the equivalent operation performed
through an open incision. 27 In terms of endocrine balance, the greatest difference
between open and laparoscopic surgery is the more rapid equilibration of most stress-
mediated hormone levels after laparoscopic surgery. Immune suppression also is less
after laparoscopy than after open surgery. There is a trend toward more rapid
normalization of cytokine levels after a laparoscopic procedure than after the equivalent
procedure performed by celiotomy. 28

Transhiatal mobilization of the thoracic esophagus is commonly performed as a
component of many laparoscopic upper abdominal procedures. Entering the posterior
mediastinum transhiatally exposes the thoracic organs to positive insufflation pressure
and may result in decreased venous return and a resultant decrease in cardiac output. If
there is compromise of the mediastinal pleura with resultant CO2 pneumothorax, the
defect should be enlarged so as to prevent a tension pneumothorax.




                                                                             Page 3 |   s   x x
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? Surg
Endosc 9:501, 1995. [PMID: 7676370]

10. Tsereteli Z, Terry ML, et al: Prospective randomized clinical trial comparing nitrous oxide and carbon
dioxide 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): Baillière's Clinical
Gastroenterology: Laparoscopic Surgery. London/Philadelphia: Baillière Tindall, 1993, p 757.

12. Ho HS, Gunther RA, et al: Intraperitoneal carbon dioxide insufflation and cardiopulmonary functions. Arch
Surg 127:928, 1992. [PMID: 1386506]

13. Wittgen CM, Andrus CH, et al: Analysis of the hemodynamic and ventilatory effects of laparoscopic
cholecystectomy. 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 haemodynamic
function 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. Br
J Anaesth 56:1213, 1984. [PMID: 6237663]

17. Borten M, Friedman EA: Choice of anaesthesia, in Laparoscopic Complications: Prevention and
Management. 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, Gossot
D, 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 Res
30:249, 1981. [PMID: 7230773]

22. McDougall EM, Monk TG, Wolf JS Jr., et al: The effect of prolonged pneumoperitoneum on renal function
in 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
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 during
laparoscopic 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 Anesth
2:129, 1990. [PMID: 2140690]

26. Alijani A, Cuschieri A: Abdominal wall lift systems in laparoscopic surgery: Gasless and low-pressure
systems. Semin Laparosc Surg 8:53, 2001. [PMID: 11337737]

27. Ozawa A, Konishi F, Nagai H, et al: Cytokine and hormonal responses in laparoscopic-assisted colectomy
and 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 open
liver resection. Surg Endosc 16:899, 2002. [PMID: 12163951]


                                                            Source: Schwartz's Principles of Surgery




www.SAWA2006.com                                                                            Page 5 |   s    x x

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Laparoscopy pathophysiology by ma3en abu 7oseh

  • 1. Laparoscopic Surgery Pathophysiology The unique feature of endoscopic surgery in the peritoneal cavity is the need to lift the abdominal wall from the abdominal organs. Two methods have been devised for achieving this.7 The first, used by most surgeons, is the induction of a pneumoperitoneum. Throughout the early twentieth century intraperitoneal visualization was achieved by inflating the abdominal cavity with air, using a sphygmomanometer bulb. 8 The problem with using air insufflation is that nitrogen is poorly soluble in blood and is slowly absorbed across the peritoneal surfaces. Air pneumoperitoneum was believed to be more painful than nitrous oxide pneumoperitoneum but less painful than carbon dioxide pneumoperitoneum. Subsequently, carbon dioxide and nitrous oxide were used for inflating the abdomen. N2O had the advantage of being physiologically inert and rapidly absorbed. It also provided better analgesia for laparoscopy performed under local anesthesia when compared with CO2 or air. 9 Despite initial concerns that N2O would not suppress combustion, controlled clinical trials have established its safety within the peritoneal cavity. 10 In addition, nitrous oxide has recently been shown to reduce the intraoperative end-tidal CO2 and minute ventilation required to maintain homeostasis when compared to CO2 pneumoperitoneum. 10 The effect of N2O on tumor biology and the development of port site metastasis are unknown. As such, caution should be exercised when performing laparoscopic cancer surgery with this agent. Finally, the safety 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 absorbed across the peritoneal membrane into the circulation. In the circulation, CO 2 creates a respiratory acidosis by the generation of carbonic acid. 11 Body buffers, the largest reserve of which lies in bone, absorb CO2 (up to 120 L) and minimize the development of hypercarbia or respiratory acidosis during brief endoscopic procedures. 11 Once the body buffers are saturated, respiratory acidosis develops rapidly, and the respiratory system assumes the burden of keeping up with the absorption of CO2 and its release from these buffers. In patients with normal respiratory function this is not difficult; the anesthesiologist increases the ventilatory rate or vital capacity on the ventilator. If the respiratory rate required exceeds 20 breaths per minute, there may be less efficient gas exchange and increasing hypercarbia. 12 Conversely, if vital capacity is increased substantially, there is a greater opportunity for barotrauma and greater respiratory motion–induced disruption of the upper abdominal operative field. In some situations it is advisable to evacuate the pneumoperitoneum or reduce the intra-abdominal pressure to allow time for the anesthesiologist to adjust for hypercarbia. 13 While mild respiratory acidosis probably is an insignificant problem, more severe respiratory acidosis leading to cardiac arrhythmias has been reported. 14 Hypercarbia also causes tachycardia and increased systemic vascular resistance, which elevates blood pressure and increases myocardial oxygen demand. 11,14 Page 1 | s x x
  • 2. The pressure effects of the pneumoperitoneum on cardiovascular physiology also have been studied. In the hypovolemic individual, excessive pressure on the inferior vena cava and a reverse Trendelenburg position with loss of lower extremity muscle tone may cause decreased venous return and cardiac output. 11,15 This is not seen in the normovolemic patient. The most common arrhythmia created by laparoscopy is bradycardia. A rapid stretch of the peritoneal membrane often causes a vagovagal response with bradycardia and occasionally hypotension. 16 The appropriate management of this event is desufflation of the abdomen, administration of vagolytic agents (e.g., atropine), and adequate volume replacement. 17 With the increased intra-abdominal pressure compressing the inferior vena cava, there is diminished venous return from the lower extremities. This has been well documented in the patient placed in the reverse Trendelenburg position for upper abdominal operations. Venous engorgement and decreased venous return promote venous thrombosis. 18,19 Many series of advanced laparoscopic procedures in which deep venous thrombosis (DVT) prophylaxis was not used demonstrate the frequency of pulmonary embolus. This usually is an avoidable complication with the use of sequential compression stockings, subcutaneous heparin, or low-molecular-weight heparin. 20 In short-duration laparoscopic procedures, such as appendectomy, hernia repair, or cholecystectomy, the risk of DVT may not be sufficient to warrant extensive DVT prophylaxis. The increased pressure of the pneumoperitoneum is transmitted directly across the paralyzed diaphragm to the thoracic cavity, creating increased central venous pressure and 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 well maintained. 19,20,21 The direct effect of the pneumoperitoneum on increasing intrathoracic pressure increases peak inspiratory pressure, pressure across the chest wall, and also the likelihood of barotrauma. Despite these concerns, disruption of blebs and consequent pneumothoraces are rare after uncomplicated laparoscopic surgery. 21 Increased intra-abdominal pressure decreases renal blood flow, glomerular filtration rate, and urine output. These effects may be mediated by direct pressure on the kidney and the renal vein. 22,23 The secondary effect of decreased renal blood flow is to increase plasma renin release, thereby increasing sodium retention. Increased circulating antidiuretic hormone (ADH) levels also are found during the pneumoperitoneum, increasing free water reabsorption in the distal tubules. 24 Although the effects of the pneumoperitoneum on renal blood flow are immediately reversible, the hormonally mediated changes, such as elevated ADH levels, decrease urine output for up to 1 hour after the procedure has ended. Intraoperative oliguria is common during laparoscopy, but the urine output is not a reflection of intravascular volume status; intravenous fluid administration during an uncomplicated laparoscopic procedure should not be linked to urine output. Because fluid losses through the open abdomen are eliminated with laparoscopy, the need for supplemental fluid during a laparoscopic surgical procedure is rare. The hemodynamic and metabolic consequences of pneumoperitoneum are well tolerated by healthy individuals for a prolonged period and by most individuals for at least a short period. 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 alternative approaches should be considered or insufflation pressure reduced. Alternative gases that have been suggested for laparoscopy include the inert gases helium, neon, and argon. These gases are appealing because they cause no metabolic effects, but are poorly soluble in blood (unlike CO2 and N2O) and are prone to create gas emboli if the gas has direct access to the venous system. 19 Gas emboli are rare but serious complications of laparoscopic surgery. 20,25 They should be suspected if hypotension develops during insufflation. Diagnosis may be made by listening (with an esophageal stethoscope) for the characteristic "mill wheel" murmur. The treatment of gas embolism is to place the patient in a left lateral decubitus position with the head down to trap the gas in the apex of the right ventricle. 20 A rapidly placed central venous catheter then can be used to aspirate the gas out of the right ventricle. In some situations minimally-invasive abdominal surgery should be performed without insufflation. This has led to the development of an abdominal lift device that can be placed through a 10- to 12-mm trocar at the umbilicus. 26 These devices have the advantage of creating little physiologic derangement, but they are bulky and intrusive. The exposure and working room offered by lift devices also are inferior to those accomplished by pneumoperitoneum. Lifting the anterior abdominal wall causes a "pinching in" of the lateral flank walls, displacing the bowel medially and anteriorly into the operative field. A pneumoperitoneum, with its well-distributed intra-abdominal pressure, provides better exposure. Abdominal lift devices also cause more postoperative 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 lessened with laparoscopic surgery, but this is not always the case. Serum cortisol levels after laparoscopic operations are often higher than after the equivalent operation performed through an open incision. 27 In terms of endocrine balance, the greatest difference between open and laparoscopic surgery is the more rapid equilibration of most stress- mediated hormone levels after laparoscopic surgery. Immune suppression also is less after laparoscopy than after open surgery. There is a trend toward more rapid normalization of cytokine levels after a laparoscopic procedure than after the equivalent procedure performed by celiotomy. 28 Transhiatal mobilization of the thoracic esophagus is commonly performed as a component of many laparoscopic upper abdominal procedures. Entering the posterior mediastinum transhiatally exposes the thoracic organs to positive insufflation pressure and may result in decreased venous return and a resultant decrease in cardiac output. If there is compromise of the mediastinal pleura with resultant CO2 pneumothorax, the defect 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? Surg Endosc 9:501, 1995. [PMID: 7676370] 10. Tsereteli Z, Terry ML, et al: Prospective randomized clinical trial comparing nitrous oxide and carbon dioxide 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): Baillière's Clinical Gastroenterology: Laparoscopic Surgery. London/Philadelphia: Baillière Tindall, 1993, p 757. 12. Ho HS, Gunther RA, et al: Intraperitoneal carbon dioxide insufflation and cardiopulmonary functions. Arch Surg 127:928, 1992. [PMID: 1386506] 13. Wittgen CM, Andrus CH, et al: Analysis of the hemodynamic and ventilatory effects of laparoscopic cholecystectomy. 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 haemodynamic function 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. Br J Anaesth 56:1213, 1984. [PMID: 6237663] 17. Borten M, Friedman EA: Choice of anaesthesia, in Laparoscopic Complications: Prevention and Management. 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, Gossot D, 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 Res 30:249, 1981. [PMID: 7230773] 22. McDougall EM, Monk TG, Wolf JS Jr., et al: The effect of prolonged pneumoperitoneum on renal function in 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 during laparoscopic 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 Anesth 2:129, 1990. [PMID: 2140690] 26. Alijani A, Cuschieri A: Abdominal wall lift systems in laparoscopic surgery: Gasless and low-pressure systems. Semin Laparosc Surg 8:53, 2001. [PMID: 11337737] 27. Ozawa A, Konishi F, Nagai H, et al: Cytokine and hormonal responses in laparoscopic-assisted colectomy and 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 open liver resection. Surg Endosc 16:899, 2002. [PMID: 12163951] Source: Schwartz's Principles of Surgery www.SAWA2006.com Page 5 | s x x