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SURGICAL WEBSITES             KIDNEY SURGERY         POSTGRADUATE SURGERY LINKS 

BREAST DISEASE     Breast cancer Breast lump Breast awareness Breast calcifications  Breast cysts Breast pain Duct ectasia Fat necrosis Fibroadenoma Hyperplasia Intraductal papilloma Phyllodes tumour Sclerosing adenosis                                                                                                                                                 

LIVER ABSCESS      Anatomy of liver Physiology of liver Method of examination of liver Haematology of liver disease. Amoebic liver abscess .Pyogenic liver abscess. Percutaneous needle aspiration of liver abscess. Case study.  Result Result continued  Discussion                                                                 

CHOLECYSTECTOMY    Introduction   Historical Review  Anatomy of Gallbladder Physiology of Gallbladder Physiologic effects of pneumoperitoneum Pathology  of Gallbladder Investigations Pre- operative preparation of laparoscopic cholecystectomy Contraindications  Treatment modalities for gallstones.  Anaesthesia                                                                                                                       

INGUINAL HERNIA    HOW SURGICAL OPERATION IS DONE     THYROID EXAMINATION MANAGEMENT OF SEVERELY INJURED PATIENT      SEPSIS AND MULTIPLE ORGAN FAILURE CHEST TRAUMA     BRONCHOGENIC CARCINOMA     TETANUS AND ANAEROBIC INFECTIONS 

PHYSIOLOGIC EFFECTS OF PNEUMOPERITONEUM.

                                      

      Laparoscopy requires the establishment of pneumoperitoneum in order to provide adequate surgical exposure and maintain operative freedom. Insufflation of carbondioxide into the peritoneal cavity however, can affect several haemostatic systems, leading to alterations in acid base balance, blood gases and cardiovascular and pulmonary physiology. Although healthy individuals may well tolerate these changes, they may increase physiological stress in patients with pre-existing condition, placing them at increased risk of perioperative complications. An understanding of the physiological changes caused by carboperitoneum is therefore essential for identification of high-risk patients and formulation of accurate treatment plans, which may include preoperative optimisation and perioperative monitoring.

      The creation of the pneumoperitoneum is a complex physiological event with the changes in physiochemical environment of the peritoneal space affecting a number of other haemostatic symptoms. Although it would seem evident that elderly, disabled patients might benefit greatly from the reduction in surgical trauma by laparoscopy, they may be at increased risk for perioperative complications due to haemodynamic and cardiorespiratory changes caused by pneumoperitoneum. Treatment decisions for potential high-risk patients undergoing laparoscopic surgery therefore require an understanding of these changes. Patients who may be at increased risk for complications can then be identified and appropriate measures can then be taken to ensure optimal perioperative support and outcome.

 

BLOOD GAS AND ACID-BASE METABOLISM.

      Carbon dioxide is currently the most commonly used gas for creating pneumoperitoneum. As a non-combustible gas, carbondioxide is safe to use with electrosurgical devices and its solubility in blood and reactivity with soluble buffering system minimises the risk of gas emboli. Significant elevation in serum levels of CO₂ (pCO₂) or end tidal CO₂ levels along with a concomitant fall in serum pH levels, have been observed during CO₂ pneumoperitoneum ³².

Hypercarbia is primarily due to transperitoneal absorption of intraperitoneal CO₂. Insufflation of CO₂ causes hyperventilation presumably to maintain normocarbia. Disturbance in the CO₂  homeostasis of sufficient magnitude so as to become clinically problematic seem to occur mainly in patients with underlying disabilities. In particular, severe cardiac or pulmonary disease has been associated with the development of more profound hypercarbia and acidaemia during carboperitoneum that would be otherwise be seen in patients with normal cardiopulmonary function. CO₂ is a product of normal cellular respiration, which, because of its high diffusion capacity, rapidly moves between body compartments along small concentration gradients. After passing through the cell membrane into the interstitial space, CO₂ enters the vascular compartment at the capillary level. The gas is then transported to the lung where it is eliminated by ventilation. Under normal circumstances, local tissue or plasma CO₂ concentration is dependent upon a number of variables, including cellular metabolism, local tissue perfusion, regional blood flow and ventilatory capacity. Once the pneumoperitoneum is established the flux of the exogenous CO₂ becomes an additional variable. For most healthy patients, the introduction of intra peritoneal CO₂ causes clinically insignificant changes in CO₂ homeostasis, manifested by mild hypercarbia and an increased in measured CO₂ production. These individuals probably adapt to extra CO₂ by maximising plasma and intra cellular buffering system and accelerating CO₂ transport and elimination. In other patients the homeostatic reserve may be limited and easily overwhelmed by increased CO₂ load, placing them at a risk of developing more severe hypercarbia and acidosis. This includes patients with a high metabolic and cellular respiratory rates, impaired regional blood flow, a large respiratory “dead space” (i.e., patients with chronic obstructive airway disease), or poor cardiac output. During laparoscopy, the patients of these categories requires close monitoring of their cardiorespiratory parameters, since the development of significant hypercarbia and acidaemia may increase the potential for secondary changes in cardiovascular function and exacerbate pre-existing cardiovascular dysfunction.

      With respect of changes in oxygenation, the effect of pneumoperitoneum appears to be small and clinically unimportant. There is a minor decrease in arterial pO₂, which was significantly greater in patients who had mechanical ventilation, presumably due to decreased gas exchange at the lung bases. Change of position of the patient has an effect on arterial pO₂ ³³. Theler et al has demonstrated that there is no significant change in pH in patients undergoing laparoscopic cholecystectomy ³⁴.

 

HYPERKALAEMIA:

      Translocation of potassium from intracellular to extracellular fluid my follow tissue damage and hypoxia. Ischemic damage to the muscles of the abdominal wall may have occurred as increased intraabdominal pressure has been shown to cause a significant reduction in abdominal wall blood flow. It is unlikely however that this mechanism alone would have caused the observed changes in plasma potassium. Oligouric renal failure associated with intraabdominal pressures between 2.00 and 2.67 kPa has been described ³⁵. The association between renal failure and hypokalaemia is well known. The rate of increase in the potassium concentration suggests that the mechanism alone is insufficient to be solely responsible.

      Another possible cause is the diffusion of carbon dioxide out of the peritoneal cavity producing local intracellular acidosis sufficient to cause movement of intracellular potassium into the blood. If pneumoperitoneum were to continue beyond 3 hours the plasma potassium concentration might well increase to a level at which immediate treatment is recommended ³⁶.

      In addition to this progressive hypokalaemia can be caused by Suxamethonium and use of I/V fluids containing potassium.

 

PULMONARY MECHANICS

            Changes in pulmonary physiology during laparoscopy are almost entirely mechanical and primarily due to pneumoperitoneum, with lesser effects arising from changes in position. Peritoneal Insufflation increases both intra abdominal pressure and intra-abdominal volume, both of which impede diaphragmatic excursion ³⁷. As a result peak airway pressure rises, whereas pulmonary compliance and vital capacity falls ³⁸. Use of Trendelenberg position seems to have little added effect and does not appear to exacerbate the rise in airway pressures ³⁹. The increase in the intraperitoneal volume can displace the diaphragm into the thoracic cavity, compressing the basilar lung segment. Physiologically this is manifested as a decrease in functional residual capacity with an increase in alveolar dead space and resultant ventilation / perfusion (V/Q) mismatch and probably accounts for the relative hypoxaemia seen in patients allowed to breath spontaneously during laparoscopic procedures. The increase in intra-abdominal pressure is also transmitted across the diaphragm causing a smaller but proportionate rise in the intrathoracic pressure ⁴⁰. The increase in the intra-thoracic pressure may exacerbate gastro-oesophageal reflux in predisposed patients, placing them at a higher risk of aspiration if the airway is unprotected. There is a more prolonged reduction in respiratory muscle function and this is likely to contribute respiratory complications in patients under going laparoscopic cholecystectomy ⁴¹. Although laparoscopic cholecystectomy does not increase metabolic demands in the early postoperative period, it impairs diaphragm function. The internal site of surgical intervention appears to be the critical variable determining diaphragmatic inhibition after laparoscopic abdominal surgery ⁴².

 

CARDIOVASCULAR PERFORMANCE

      Pneumoperitoneum may affect cardiovascular performance as a result of an increase in pCO₂ concentration or due to the elevation of the intraperitoneal pressure. Moderate to severe hypercarbia can alter cardiovascular function through both primary interactions with myocardial and smooth muscle and secondary autonomically mediated changes ⁴³. Increasing pCO₂ to 55-70 mm Hg may cause elevation in heart rate, systolic blood pressure, central venous pressure, cardiac output, and stroke volume with decrease in peripheral vascular resistance. Elevation in plasma catecholamine levels is also observed. Since the direct effect of the hypercarbia include arteriolar dilatation and myocardial depression, the overall change in cardiac function is thought to be mediated by catecholamine release with b-adrenergic effect predominating.

      Mild hypercarbia (pCO₂ of 45 to 50 mmHg), however, appears to have little impact on haemodynamic function. This distinction is clinically important since elevation of pCO₂ observed during uncomplicated carboperitoneum in healthy patients rarely exceeds this level. Spontaneous respiration did lead to significant rise in pCO₂  significant elevations in blood pressure were observed after pneumoperitoneum.

      When intraperitoneal pressure was raised to 30mmHg, CVP decreases significantly from previous levels ⁴⁴.

 

GAS EMBOLISM:

      Gas embolus formation, although rare has been reported during laparoscopy. Carbondioxide embolim occurs most frequently in the initial phase of laparoscopic procedure. Intravascular gas insufflation after inadverent puncture of intra abdominal vessels, accidental insertion of trocar into the liver before laparoscopic cholecystectomy have been reported causes of carbondioxide embolism ⁴⁵. Gas embolism can occur any time during the procedure as a consequence of an open venous channel and a pressure gradient between abdominal cavity and the venous system ⁴⁶.

      CO₂ embolism should be considered in the event of the acute cardiovascular collapse or an appearance of an otherwise unexplained malignant dysrthymia during pneumoperitoneum. The presence of characteristic ‘mill wheel” murmur may be of assistance in making the diagnosis. It may proceed to adult respiratory distress syndrome like syndrome leading to hypoxaemia and dramatic reduction in pulmonary compliance.

 

SUBCUTANEOUS EMPHYSEMA:

      Massive subcutaneous emphysema during pneumoperitoneum has been reported, presumably due to extravasation of intraperitoneal gas into soft tissues. The subcutaneous gas expands CO₂ stores with the entire body thereafter acting as CO₂ “sink.” If enough CO₂ is sequestered in soft tissues, total CO₂ excretion may overwhelm endogenous clearance mechanisms requiring prolonged mechanical ventilation to support hyperventilation in order to avoid hypercarbia, acidosis and CO₂ narcosis until the gas is cleared.

 

METABOLIC AND IMMUNE RESPONSES ASSOCIATED WITH LAPAROSCOPIC CHOLECYSTECTOMY.

Laparoscopic cholecystectomy has become the operation of choice for uncomplicated gallstones. Increase recovery occurs with decrease discomfort, resulting from small skin incision and an early discharge. Laparoscopic approach also improves per operative respiratory function and it has been postulated that the absence of a large wound may diminish the catabolic response to surgery.

Elective surgical wound elicit physiological responses mediated via afferent neural stimuli and circulating factors. In addition insufflation of the peritoneal cavity during laparoscopic cholecystectomy is associated with painful abdominal and diaphragmatic stimuli, with tachycardia and increase in blood pressure, the characteristic of a sympathetic response.  The attenuation of these responses can be detrimental if excessive.

Epidural anaesthesia can block the afferent neural stimuli of surgical wound. But controlling the circulating factors as hormones, cytokines, leukotrienes ecosanoid and prostanoid mediators are difficult to achieve.

Laparoscopic cholecystectomy provides an alternative approach to diminish the above responses, by avoidance of a substantial abdominal incision - the site of maximum tissue damage. These physiological and metabolic responses and the effect of laparoscopic surgery on them are evaluated below.

(1) METABOLIC RESPONSES:

Metabolic and inflammatory responses and changes in fatigue were studied in patients undergoing either laparoscopic cholecystectomy. The mean (s.e.m.) cortisol concentration was significantly increased after surgery. Glucose concentration was increased at the end of surgery. The mean glucose concentration during the initial 12 h after surgery was significantly greater. The mean (s.e.m.) albumin concentration fell significantly during surgery by an equivalent extent. The mean interleukin (IL) 6 concentration peaked 4 h after surgery. Mean (95 per cent confidence interval) C-reactive protein (CRP) levels at 24 h were higher at 48 h. Mean (s.e.m.) fatigue scores were significantly increased from preoperative values at 24 h after laparoscopic. These results demonstrate that aspects of the metabolic and acute-phase responses are attenuated following laparoscopic cholecystectomy, consistent with a reduction in tissue trauma. ⁴⁷.

 

(2) IMMUNE RESPONSES:

Laparoscopic cholecystectomy does not significantly alter parameter of immunocompetence nor interferes with cellular immune function. The advantages of laparoscopic cholecystectomy over the open procedure seem to be related to the lesser surgical trauma. This is also reflected by reduced postoperative immune suppression. The perioperative cellular immunocompetence of patients undergoing either laparoscopic or open cholecystectomy was evaluated before operation and at 24 hours and 6 days after operation for inflammatory reactivity by white blood cell counting and serum interleukin-6 assessment. Immunocompetence was evaluated by skin testing with phytohemagglutinin and by phenotyping blood mononuclear cells. Although 24 hours after conventional cholecystectomy granulocyte and interleukin-6 levels were strongly increased, laparoscopic cholecystectomy did not affect these acute inflammation parameters. Patients who had undergone conventional cholecystectomy showed a strong reduction of phytohemagglutinin responsiveness, in contrast to laparoscopic patients. Flow cytometric analysis of blood mononuclear cells revealed a distinct reduction of HLA-DR expression on monocytes in the open cholecystectomy group only. Both parameters returned to baseline levels within 6 days after operation. In contrast to open cholecystectomy, laparoscopic cholecystectomy does not significantly affect parameters reflecting immunocompetence. This lack of interference with cellular immune functions provides another argument favouring laparoscopic rather than open cholecystectomy ⁴⁸. A prospective study by Redmond et al showed, abnormal release of inflammatory mediators following surgical injury is associated with immunological alteration, which may predispose to sepsis. Laparoscopic surgery is associated with reduced postoperative complications, but mechanisms are unclear. It is hypothesised that early recovery following laparoscopic surgery may relate to minimal impairment of immune function. Immune parameters, including monocyte superoxide anion (O₂^-) and tumour necrosis factor release, neutrophil O₂^- levels and chemotaxis, total white blood cell counts, partial arterial oxygen pressure, and serum cortisol and C-reactive protein levels were assessed preoperatively and on postoperative days 1 and 3 and significant increases in monocyte release of O₂^- and tumour necrosis factor, neutrophil release of O₂^- and chemotaxis, and white blood cell count in the open Vs laparoscopic cholecystectomy study groups, with a concomitant decrease in partial arterial oxygen pressure. These findings correlated with significantly higher postoperative septic complications in the open cholecystectomy group. There were no significant differences in either plasma cortisol or C-reactive protein levels between groups. Laparoscopic surgery appears to be associated with similar metabolic responses compared with open surgery, while immune parameters vary greatly between groups. The beneficial effects of laparoscopic surgery may relate, in part, to preservation of immune function in the postoperative period ⁴⁹. Immune activity [neutrophils, total lymphocytes count, lymphocytes subpopulations, human leukocyte antigen-DR (HLA-DR)] is altered. Monocyte antigen HLA-DR was reduced in patients with "open" cholecystectomy. In conclusion, laparoscopic cholecystectomy avoids. immunosuppression, mostly due to conservation of HLA-DR activity, with less postoperative morbidity compared to that seen with open surgery.

POST OPERATIVE FATIGUE:

Aetiological factors in postoperative fatigue and muscle weakness include muscular inactivity, fasting and changes in intermediate metabolism as a consequence of trauma. A reduction in any of these might diminish postoperative fatigue and contribute to early recovery. Reduced fatigue occurs in laparoscopic compared with open cholecystectomy in the initial 48 hours. This may be explained, in part by the difference in the acute phase responses.

The above reviews on physiological and metabolic responses on laparoscopic cholecystectomy indicate improved respiratory and subjective responses diminished acute phase responses, associated with laparoscopic cholecystectomy. Although catabolic hormone release may however be increased.

Laparoscopic cholecystectomy does not significantly alter parameter of immunocompetence nor interferes with cellular immune function.

 

STRESS HORMONES:

In many retrospective and prospective observational studies, laparoscopic cholecystectomy compares favorably with conventional cholecystectomy, with respect to length of hospital stay, postoperative pain, and pulmonary function, indicating a diminished operative trauma. Comparison of laboratory findings (stress hormones, blood glucose, interleukins) are a possibility to objectify stress and tissue trauma of laparoscopic and conventional cholecystectomy. Major body injury, surgical or accidental, evokes reproducible hormonal and immunologic responses. The magnitude of many of these changes essentially is proportional to the extent of the injury. Significantly lower values of intraoperatively and postoperatively measured epinephrine, norepinephrine, interleukin-1 beta, and interleukin-6 are found in patients with laparoscopic cholecystectomy, indicating a minor stress response and tissue trauma in this group of patients. The results correspond to the favorable results of most other trials evaluating clinical aspects of laparoscopic cholecystectomy. ⁵⁰.

Increase in plasma renin activity and noradrenaline concentration occur in response to carbon dioxide insufflation during laparoscopic cholecystectomy. The abdominal wall lift method with minimal carbon dioxide insufflation was associated with smaller neuroendocrine responses and better preservation of renal function compared with conventional carbon dioxide pneumoperitoneum ⁵¹. Cortisol, adrenaline and noradrenaline oppose the action of insulin and promote muscle catabolism. Levels of both these hormones are increased after major surgery. Urinary products of cortisol and adrenaline measured showed increase in laparoscopic than open cholecystectomy suggesting significant stress response. High level of vinylmandelic acid in urine may be due to afferent neural stimuli from the pneumoperitoneum.

HEPATIC ACUTE PHASE PROTEIN:

Acute phase proteins increase from surgery, trauma and sepsis. C-reactive protein is a major component of the acute - phase response. Post operative C-reactive protein levels at 24 and 48 hours were raised more in open cholecystectomy than laparoscopic, indicating a greater inflammatory response in open. Acute phase proteins are released into the circulation as part of the metabolic response to trauma. C reactive protein has been shown to be the most specific and sensitive indicator of trauma. Pre- and postoperative C-reactive protein levels were laparoscopic cholecystectomy and open cholecystectomy. A difference is shown in the C-reactive protein levels between open and laparoscopic cholecystectomy ⁵². Extraperitoneal tumour growth was significantly accelerated after laparotomy and correlated with significantly suppressed natural killer and lymphokine activated killer cytotoxicity for at least 4 days after operation. Laparoscopy had a shorter, less profound effect on tumour growth and immune function ⁵³.

 

(3) HAEMODYNAMIC CHANGES:

Alteration in fluid balance and in intermediate metabolism occurs in all patients undergoing surgery. Haemodynamic changes measured in patients during laparoscopic cholecystectomy by transthoracic electrical bioimpedance showed, “Insufflation resulted in a mean decrease in stroke index, effect an cardiac index was more variable, mean arterial pressure increased and systemic vascular resistance index increased, with the maximum effect occurring 10-15 minutes after the commencement of insufflation. Insufflation pressure significantly affects the haemodynamic changes and postoperative pain associated with laparoscopic cholecystectomy ⁵⁴.

Haemodynamic changes associated with insufflation and the reverse Trendelenburg's position include, increase in left ventricular end systolic wall stress, left ventricular end diastolic area decreased after reverse Trendelenburg's position. Left ventricular ejection fraction was maintained.

 

(4) NEGATIVE NITROGEN BALANCE:

It reflects the erosion of lean body mass. No significant change was seen in laparoscopic cholecystectomy as compared to open procedure in urinary nitrogen over 24 hours duration, although early oral intake in laparoscopic cholecystectomy does influence nitrogen balance in favour of laparoscopic group than open.