Jacobs Journal of Anesthesiology and Research

Anesthetic Management of Laparoscopic Surgery in Obese Patients

* Bret D. Alvis
Department Of Anesthesiology, Vanderbilt University Medical Center, United States

*Corresponding Author:
Bret D. Alvis
Department Of Anesthesiology, Vanderbilt University Medical Center, United States

Published on: 2018-08-24


Obesity is a situation increasing globally, evaluated as a disease and which creates serious health risks. Obese patients may encounter serious difficulties with mask ventilation and intubation during anesthesia. Body mass index (BMI) is mainly used for the definition of obesity. However, in definition of obesity BMI is insufficient and the fat distribution pattern around the waist line is a better indicator. Obesity causes significant changes in metabolic, cardiovascular and pulmonary functions and these changes increase anesthesia risks. A successful anesthesia method for laparoscopic interventions in obese patients requires coordinated team work involving multiple disciplines and well-designed care. To ensure the best results and reduce complications, it is important to deal with the changed physiology of these types of patients. In this review our aim is to determine an approach to preoperative evaluation, general anesthesia, laparoscopic procedures and postoperative complications and intensive care of obese patients in light of the literature.


obesity; anesthesia; laparoscopy


Obesity is a proinflammatory multisystemic disease defined as an increase in diameter of cells (hypertrophy) and/or numbers of cells (hyperplasia) in fat storage. The body mass index (BMI) is used in the definition of obesity. Body mass index 30 kg/m2 is obese, BMI >40 kg/m2 or BMI >35 kg/m2 and accompanying disease (like hypertension, diabetes mellitus) is defined as morbid obesity. Additionally obesity may be named according to anatomic distribution of fat tissue. In patients with fat around the abdominal region it is android type, whereas patients with fat distributed around the hips and legs have gynecoid type obesity. According to research, in our country 26.4% of the adult male population and 38.5% of the female population are obese. Parallel to the increase in BMI in obesity, the risk of both difficult airway management, and accompanying diseases increasing morbidity and mortality such as hypertension, diabetes mellitus, coronary artery disease and congestive heart failure and respiratory problems increases. Increased basal metabolic rate, high oxygen consumption and carbon dioxide production make patients more susceptible to rapid desaturation3.Obese patients may encounter severe difficulties with mask ventilation and intubation during anesthesia. Additionally the distribution volume and elimination of medications used may change in the body. All these factors affect the approach of anesthesiologists to obese patients. During perioperative management of obese patients, for high chance of success and low complication rates, team work is required [4].

I. Physiological Changes in Obesity

Obesity is an increasing clinical problem for anesthesiologists. The incidence of obesity has continued to increase in the last few decades and is calculated to be nearly 27% [1, 5]. Obesity increases the risks for many diseases including diabetes mellitus (DM), coronary artery disease (CAD), obstructive sleep apnea (OSAS), hypertension (HT) and degenerative joint diseases. Morbid obesity is related to many physiological disorders and may cause many accompanying diseases. All of these must be appropriate before elective surgery and necessary intraoperative conditions should be ensured. Obesity causes physiological and pathological changes affecting all organ systems differently to individuals with normal weight. As a result the changes occurring in the body will be investigated [6, 7]. 

Respiratory System Changes

The changes involving the upper respiratory tract include: short and thick neck, increased pharyngeal and palatal soft tissue. Linked to these narrowing of the respiratory tract is observed and the tongue is large. Due to increased weight the larynx is relocated forward and upward [7, 8]. To meet the excess metabolic requirements, oxygen consumption, carbon dioxide production and alveolar ventilation increases. Respiratory workload increases and efficiency reduces. Due to excess fat tissue on the thorax, diaphragm movement becomes difficult and thorax compliance and lung compliance decreases. Increased abdominal fat mass pushes the diaphragm up and reduces lung volume [9]. Functional residual capacity reduces, expiratory reserve volume, vital capacity (VC) and total lung capacity reduce. These findings indicate restrictive lung disease. Together with this, respiratory workload, oxygen consumption, CO2 production and V/Q incompliance increase. These conditions cause rapid denaturation. These situations cause rapid desaturation within 1 to 2 minutes [10]. Obesity increases the risk of OSAS, obesity hypoventilation syndrome (OHS, a result of OSA in the long term) and pulmonary hypertension. According to estimates 60-90% of OSA patients are obese and the majority of cases are undiagnosed. [11].

Circulatory System Changes

To both perfuse and carry increased fat tissue the cardiac output of obese patients increases. In addition to total blood and plasma volume, the workload on the heart and cardiac output increases. Blood pressure rises (HT). Pulse is generally normal. Severe hypertension is observed in 5-10% of obese patients and moderate hypertension in 50%. The risk of left heart failure, coronary artery disease and cerebrovascular events increases linked to increased cardiac output. Pulmonary hypertension may develop. The risk of cardiomyopathy and coronary artery disease increases in obesity. Additionally arrhythmia, hypoxia, left atrial-ventricular dilatation, catecholamine increase and hypercapnia is observed. Also for hypercoagulation the VTE incidence is 10 times higher in women and may extend over 2 weeks postop [12-15]. Fat distribution around the waist of >90-94 cm in males and >75-80 cm in females increases the risk of perioperative metabolic and cardiovascular complications. Waist circumference >120 cm in males and >110 cm in females in those above 50 years of age increases the mortality risk [16].

Endocrine and Metabolic System Changes

Increased free fatty acid level in plasma in obesity reduces leptin activity and leads to a reduction in the effect of insulin in the skeletal muscles, liver and pancreas. GLUT 4 expiration reduces and hyperglycemia develops.To tolerate this situation, hyperinsulemia develops17. As insulin resistance and hyperglycemia continue, the pancreas reserves begin to reduce and increased plasma glucose and free fatty acids cause destruction of the pancreas islet cells, negatively affecting insulin secretion and over time reducing insulin secretion and forming a diabetic tableau[17]. At the same time there is increased secretion of inflammatory cytokines like tumor necrosis factor alpha and interleukin 6 from insulin sensitive tissues and the release of anti-inflammatory mediators like adiponectin occurs [18]. It’s possible to observe the effect of diabetic development with obesity in the Framingham study. This study found that patients with BMI >35 had disrupted glucose tolerance and increased diabetes incidence compared to those with BMI<23. Together with this,fat accumulation may affect renal and endocrine functions. In obese individuals, the incidence of gallstones and cirrhosis is higher. The risk of metabolic syndrome (chronic inflammation and immune system activation) is increased. The mechanism of formation of metabolic syndrome is the disruption of lipid and glucose metabolism due to central obesity and insulin resistance [18-20].

Gastrointestinal System Changes

Intra-abdominal pressure increases in obese. At the same time,the stomach volume and acidity is greater. Hiatal hernia and gastroesophageal reflux is common. The risk of gastric aspiration and pneumonia increases. There is steatosis of the liver [21].

Pharmacological Changes

Just as they may be affected by disorders linked to accompanying diseases, the effect of fat soluble medications may directly change. The presence of hyperlipoproteinemia may affect the binding of medications to protein. The elimination time of fat-soluble anesthetics lengthens and a reduction in clearance is expected [22]. The metabolism of enflurane halothane especially increases. Volume distribution, half-life and excretion of water-soluble agents (muscle relaxants) do not change. When medications are administered in mg/kg form, care should be taken [23].

Other system changes

While the risks of both ischemic and hemorrhagic cerebrovascular events increase in males, in females though the reason is not fully known, there is an increase only in ischemic cerebrovascular disease risk [24]. For patients with weight >136 kg, the incidence of diabetes mellitus (DM) is 21%. The incidence of coronary artery disease, renal disease and cerebrovascular disease is higher in DM patients. DM increases surgical complications such as weak wound healing and infection. For those with weight >134 kg, the hypertension incidence is 44 % [25]. Hypertension increases the cardiac workload and contributes to left ventricle hypertrophy and failure [26].

The incidence of diabetes mellitus in those with BMI >40 is 7 times greater. This increases the risks of wound site infection, acute renal failure (ARF) and postoperative anastamosis leak. Non-alcoholic steatohepatitis advances to cirrhosis in 15-20 % [27]. In bariatric surgery patients, 91% are reported to have fatty liver and 37% have steatohepatitis. Mechanical and hormonal changes increase the risk of gastroesophageal reflux. Bad nutrition may affect vitamin D, magnesium, iron phosphate and vitamin A levels [28, 29]. The development of hypertension in obesity is thought to affect activation of the sympathetic system, metabolic disorders and the renin-angiotensin-aldosterone system (RAAS) [30]. Increased sympathetic activation and the high insulin and leptin levels increase renal sodium involvement, increasing renin secretion and with the RAAS activation vasoconstriction may develop [31]. Leptin causes Central nervous system -mediated thermogenesis which is necessary to maintain energy balance. Additionally the activation of the Central nervous system results in hypertension. Also due to the developing endothelial dysfunction, nitric oxide levels fall and vasoconstriction develops [32].

Obesity and Mortality

A study by Peeters et al. showing the effect of obesity on mortality reported that obese non-smoking individuals aged 40 years and older live shorter times compared to those who are not obese. According to this study, obese males live a mean of 7.1 years less than non-obese, while this value is 5.8 years for women [33]. The interheart study showed that increased fat mass at the waist circumference was related to high myocardial infarctus risk, with increasing fat distribution in the hip region having negative predictive value for myocardial infarctus [34].

II. Preoperative Evaluation in Obesity

The majority of obese patients are healthy and risks are similar to patients with normal weight. The key points are evaluation of the patient, preparation and making an anesthesia plan. Evaluation of airway, difficult intubation, OSAS history, cardiovascular system and respiratory system should be considered. It is beneficial to eat a liver-reducing diet for 2-6 weeks and to quit smoking. As the risk of gastroesophageal reflux disease (GERD) is increased in morbidly obese individuals, aspiration precautions should be considered. The weight on stress points of the joints increases and causes development of osteoarthritis. Obesity increases the risk of thromboembolic events [35]. Preoperative evaluation: No patient should be given anesthesia before a detailed airway examination is performed. It is essential to investigate previous anesthesia documents and anamnesis related to difficult airway. If intubation or ventilation is considered to be difficult, this situation should be explained to the patient and information should be given about alternative approaches like awake fiber optic intubation.

a. Respiration system; in terms of some respiratory disorders like OSAS, OHS and restrictive lung failure, airway evaluation should focus with special care on comorbid situations. Postoperative pulmonary complications are observed two times more in obese patients compared to normal ones. Changes can be identified with pulmonary function tests (PFT) for obese patients without accompanying pulmonary disease. Obesity hypoventilation syndrome (OHS) is characterized by chronic daily hypoxemia (PO2 < 65 mmHg) and hypoventilation (PCO2 > 45 mm Hg) in obese patients without COPD. These patients may develop pulmonary hypertension (PHT), right ventricle hypertrophy and right heart failure. The most logical way to observe OHS obese patients is to monitor the saturation of room air. This approach is simple, cheap and non-invasive. Arterial blood gas (ABG) analysis, carbon dioxide retention and OHS diagnosis is necessary. Polycythemia is another finding supporting hypoxemia. In OHS patients, CPAP may be beneficial. In obese patinets with hypercapnia, 2 week CPAP treatment has been beneficial to improve respiratory functions. Additionally Kaneko et al. stated that CPAP may improve cardiac functions in OSAS patients and this may be true for OHS patients [36]. Lung x-rays should show cardiomegaly and atelectasis in advanced cases.

b. Evaluation of the cardiovascular system: obese patients carry risks for venous stasis, pulmonary embolism, hypertension, cerebrovascular events, cardiomyopathy, arrhythmia and ischemic heart disease. Perioperative pulmonary embolism is one of the most important problems. During preoperative visits, determination of risk allows the opportunity for prophylaxis. Venous stasis disease, BMI >60, trunk obesity, OHS, OSAS, previous history of pulmonary embolism and hypercoagulopathy increase the risk of perioperative pulmonary embolism risk in obese patients. If risk is determined, prophylaxis should be discussed with the surgeon. Up to 60% of obese patients may have HT with tension observed to reduce when weight is lost. Frequent non-invasive blood pressure measurement may be a problem for these patients and invasive monitoring may be required. Newly-taken ECG is important. Symptomatic patients may require more advanced investigation. In these patients CAD incidence is two times greater and as myocardial infarctus is frequently encountered, ECG and exercise tolerance is beneficial to monitor perioperative events. The presence of metabolic syndrome is a risk factor.

c. Preoperative laboratory evaluation varies depending on patient and procedure, however should include the following: 1. Biochemical panel; to evaluate electrolytes, blood sugar and renal functions.

2. ECG to evaluate ventricular hypertrophy, rhythm disorders and ischemia.

3. Echocardiography is a condition to measure cardiac hypertrophy, myocardial contractility and pulmonary artery pressure. To ensure sufficient view, transesophageal echo cardiography may be required. In light of this information, anesthesiologist, patient and doctor team should discuss increased perioperative risks. Pharmacological treatment may be required for heart failure and arrhythmia. Losing weight before the operation can be effective. However, this does not succeed for many patients.

4. CBC to evaluate polycythemia.

5. Other studies like cardiac stress test and intense laboratory analyses may be required, however this is not routine [37].

d. Airway Evaluation

It is debated as to whether airway management is difficult in obese patients. Some studies have shown that it causes difficult airway and reduces perioperative cardiac functions [38]. The risk factors for difficult intubation in obese patients include wide neck circumference (NC) and high Mallampati score. NC has been found to be more reliable than weight or BMI for diagnosis of difficult airway [37, 38]. NC of nearly 44 cm is a marker of difficult intubation. Mallampati score ≥3 and neck circumference >40 cm increase the risk of difficult intubation. The difficult intubation risk was found to be 20% for neck circumference >50 cm and 35% for >60 cm. It is reported that Wilson score, NC/thyromental distance >5 are the best marker for estimation of difficult airway. Difficult intubation is reported in 15% of morbid obese patients undergoing upper airway surgery. Broad chest diameter and central distribution of weight are risk factors. Additional equipment is always required for difficult airway and preparation should be made for high risk patients. Mask ventilation for obese patients is difficult. During preoperative evaluation, potential difficult mask ventilation should be remembered. Obesity is defined as an independent risk factor for difficult mask ventilation. The patient having a beard, not having teeth and having a history of snoring increase the risk. During examination in room air, SpO2 < 95%, FVC 27 mmol/L increase the risk of anesthesia.

e. Other Evaluations;

Obesity is frequently related to GERD, and patients should be asked about this. There are no clear publications on whether the time to empty the stomach is lengthened or not. It is mostly difficult to find sufficient venous routes in obese patients. As a result, central venous catheterization may be applied [38].

Regional Anesthesia

a. To improve postoperative pain control in obese patients and reduce the use of narcotic analgesics, regional anesthesia may be beneficial. However, excess fat may make regional anesthesia difficult in these patients.

b. Reduced cerebrospinal fluid, high intra-abdominal pressure and changed respiratory physiology may increase the risk of high spinal anesthesia.

c. If spinal anesthesia is administered, careful monitoring is necessary.

d. If the optimal spinal anesthetic dose is not known, a lower dose than mean spinal dose and combined spinal epidural may be considered.

Surgery Preparation for Morbid Obese Patients

a. Weight limits of surgical table and trolleys should be checked,

b. The table should be wide enough for the patient and lengthened as necessary,

c. If a special position is necessary (e.g., Trendelenburg position), it is necessary to provide an appropriate table for the patient’s increased weight and this position [38,39].

III. General Anesthesia in Obese Patients

The most reliable technique for general anesthesia is endotracheal intubation and controlled ventilation. It is especially recommended for long laparoscopic interventions. During pneumoperitoneum, controlled ventilation should ensure Partial end-tidal carbon dioxide (PETCO2 ) values are held at nearly 35 mmHg. Depending on the study, once subcutaneous emphysema linked to CO2 does not develop, it should be sufficient to increase the respiratory count by 15-25%. In chronic obstructive pulmonary disease patients, those with history of spontaneous pneumothorax or bullous lung, rather than increasing tidal volume, increasing the rate of respiration is recommended to reduce alveolar inflation and protect against pneumothorax [39]. For obese patients operated under general anesthetic for any reason, the choice of anesthetic medications for induction and maintenance, doses, intubation difficulties, ventilation strategies for the perioperative period, fluid management, extubation and postoperative period applications are important [40]. It is possible list the points that require care in general anesthesia administration to obese patients under the following headings:

a. Premedication:

With the majority of these patients having OSAS along with obesity, respiratory depression is a situation that may cause desaturation. As a result, in the preoperative period premedication with opioids and strong sedatives should be avoided especially [41]. To reduce the risk of aspiration due to gastroesophageal reflux linked to reduced lower esophageal sphincter pressure and increased intra-abdominal pressure, it is recommended to administer particle-free antacids such as H2 receptor blockers, omeprazole, metaclopramide and sodium citrate before induction [42]. Another important topic for obese patients is the high risk of thromboembolism in both arterial and deep veins. As a result, in addition to preoperative heparin, flight socks and application of intermittent pneumatic compression, early mobilization is recommended in the postoperative period [43]. 

b. Monitoring:

In addition to standard monitoring (ECG, non-invasive blood pressure measurement, pulse oxymetry, capnography), monitoring decisions should be made depending on the extent of the procedure and accompanying situations [44]. For accurate non-invasive blood pressure measurement, it is recommended that a sleeve covering at least 75% of the arm circumference be used. In specific difficult situations and for long operations, invasive arterial monitoring and momentary pressure monitoring and if necessary arterial blood gas monitoring may be beneficial. Additionally they may be useful for neuromuscular monitoring, with facial nerve monitoring determined to be more appropriate than ulnar nerve. Catheterizing the bladder may be difficult in these patients, and finding an appropriate peripheral venous route may sometimes be impossible. Together with noting that central catheterization of these patients may be appropriate for those undergoing general anesthesia, it should not be forgotten that due to short neck jugular vein cannulation may be difficult and subclavian cannulation may be difficult due to increased fat tissue [43, 44].

c. Position and related complications:

One of the most important problems in obese patients taken for operation is determining the weight capacity of the operating table. Currently operating tables generally have capacity for 200 kg, with motorized tables having weight capacity up to 455 kg. In situations without motorized tables, two tables may be used side-by-side [45]. To provide an appropriate position for the operating table and prevent complications for these patients, trained surgery personnel are required. To protect tissues susceptible to compression, soft foam and gel pads should be used [46]. In obese patients, sciatic and ulnar nerve compression damage is more common than in normal weight patients. In addition, in some cases lumbar compartment syndrome, rhabdomyolysis can occur with muscle pressure especially in prolonged operations [47].

d. Preoxygenation and endotracheal intubation:

In obesity, increased intra-abdominal pressure, and reduction in compliance of the chest wall and lungs due to thoracic fat tissue may occur. This restrictive function disorder and increased fat tissue begins with FRC, then reduces ERV and TLC, increasing respiratory workload and oxygen consumption, increasing the formation of atelectasis [48]. In these patients position of the patient during anesthesia administration affects respiratory changes even more and with induction rapid desaturation may develop [49]. As a result providing an appropriate position for the patient on the operating table and preoxygenation carry great importance. Studies have shown that 25-30 degree head-up position increases end-expiratory volumes two-fold compared to supine position for patients under anesthesia and improves FRC, pulmonary compliance and oxygenation. This position obstructs visceral compression of the abdominal compartment, and is stated to prevent cephal movement of the diaphragm and formation of atelectasis [50, 51]. Preoxygenation may be performed in a variety of ways. Goldberg et al. stated that 4 deep breaths with 100% O2 was superior to 3 minutes continuous 100% O2 respiration [52] , while Coussa et al. reported that CPAP (continuous positive airway pressure) before induction was beneficial for PEEP administration with 10 cm- H2 O after induction and showed this on CT taken before and after induction [53]. In parallel to the BMI increase in obese patients, both mask ventilation and intubation may be difficult, and this difficulty is stated to increase in those above 55 years of age, without teeth, with a beard and with OSAS [54]. As a result, it is recommended that appropriate position be given to the patient for intubation, a second anesthesiologist should be present and equipment for difficult intubation should be ready (blades of different sizes, short handle blade, laryngeal mask, video laryngoscope, fiberoptic laryngoscope, crichothyroidectomy set, etc.) [55]. Before intubation a ramped position formed by placing raises between the shoulders and under the head can ease intubation and improve ventilation and oxygenation. In this position the tragus of the ear should be practically at the same level as the sternum [56]. 

e. Anesthesia induction and maintenance:

Together with the increase in fat tissue in obesity, the distribution volume of fat-soluble medications increases, while there may be changes in protein binding of medications due to protein and free fatty acid increases. Apart from this, blood volume, cardiac output, renal perfusion and glomerular infiltration increases and liver function disorders may affect metabolism of medication. All these reasons make the anesthetics used for anesthesia induction and maintenance and the doses used very important. In obese patients, to identify the doses for anesthetic medications, a variety of calculations are used, with no consensus on which is superior. BMI is frequently used with obesity, but a variety of calculations using definitions such as total or actual body weight (TBW), ideal body weight (IBW), and fat-free body weight (FBW) are used to determine medication dose. IBW is calculated with the formula 45.4(female)/49.9(male)+0.89×(height( cm)-152.4), while FBW is calculated as 1.07 x TBW-0.0148 × BMI ×TBW for females and 1.10×TBW-0.0128×BMI×TBW for males [57]. Again IBW is calculated as TBW-X (X is 105 for females and 100 for males) while FBW may be practically calculated as IBW + 20% [58, 59]. Due to high lipid solubility and lack of repeated dose for thiopental, it may be necessary to calculate IBW instead of TBW. For propofol, an appropriate choice for obese patients with rapid onset of effect and short effect duration, it is recommended that FBW should be used for induction while infusion should be calculated according to TBW [60]. Of benzodiazepines midozolam is most commonly used, and is recommended to be used according to IBW. Opioids are used for the majority of obese patients, with remifentanil frequently chosen due to elimination route and effect duration. It is stated that calculating remifentanil and fentanyl according to FBW, rather than TBW, is more appropriate [61]. Non-depolarizing neuromuscular blockers are mainly hydrophilic, and can be given according to IBW or FBW, while due to increasing pseudocholine activity of the depolarizing neuromuscular blocker of succinylcholine, it is more appropriately given according to TBW [62]. Atracurium and cisatracurium may be used for obese patients due to Hoffman elimination, though in recent years sugammadex which rapidly ends the effect of rocuronium is more frequently chosen for obesity, as it is for difficult intubation [62, 63]. The dose of vecuronium, rocuronium, atracurium and cisatracurium (apart from mivacurium) is determined according to IBW, while it is stated that it is necessary to avoid overdoses of vecuronium [59, 64]. Ideally neuromuscular monitoring should be performed [65]. Rather than the highly lipophilic inhalation agent of isoflurane, desflurane and sevoflurane should be chosen as they are less lipophilic and ensure rapid recovery [50, 66]. 

f. Intraoperative ventilation:

The effects of obesity and general anesthesia on the respiratory system (reduction in FRC and pulmonary compliance, increase in airway resistance) may make mechanical ventilation during operation difficult and cause frequent hypoxia. The contribution of true pulmonary shunts and atelectasis to hypoxia formation is great. Due to the harmful effects of both obesity and anesthesia, a variety of intraoperative ventilation strategies have been attempted for obese patients, however no clear superiority has been shown [67]. Respiratory frequency providing normocapnia and 6-10 ml/kg according to IBW tidal volumes has been used, 7-8 s recruitment maneuver to reach 40-45 cm H2 O plateau pressure after intubation and before extubation for hemodynamically stable patients, recruitment maneuver in the intraoperative period until extubation with 10 cm H2 O PEEP administration after each maneuver, setting the inspiration expiration ratio as 1:1 and 1:3, and giving the reverse trendelenburg position during preoxygenation and extubation periods is recommended. Before extubation to prevent resorption atelectasis it is recommended to use Fi02 values between 0.4-0.8, take care to prevent loss of PEEP during disconnection and aspiration, and to keep monitor peak pressure and airway plateau pressure ≤30 cm H2 O [68]. No superiority is reported for volume controlled or pressure controlled mode for respiration. If volume controlled ventilation is used for morbidly obese patients, if oxygenation does not improve in spite of high tidal volumes, it has been shown that this may be due to high airway pressures. These pressure values may cause damage to the lungs [69]. Pressure controlled ventilation does not guarantee tidal volume with reduced respiratory compliance and increased airway pressure, and has been shown to form a risk for hypercapnia. Whatever the method used, the main aim of intraoperative ventilation of obese patients is to ensure the alveolus and airways remain open [68, 69]. 

g. Fluid management:

As with every operation, fluid management should be performed carefully and in a balanced way for operations with obese patients. The presence of some accompanying diseases (DM, antihypertensive use including diuretics, lengthened surgical durations, rhabdomyolysis, etc.) increases the risk of postoperative renal failure; as a result it is necessary to ensure sufficient fluid replacement intraoperatively [70]. However, due to fat tissue, accessing the surgical field may be difficult, a larger surgical incision may be required and blood loss may be greater in obese patients compared to non-obese patients. As a result the importance of early infusion of blood and blood products, and colloids is emphasized However, as congestive heart failure may be observed in obese patients, it is stated that rapid fluid replacement should be avoided [71].

h. Extubation and Postoperative period:

Due to hypoxemia and atelectasis in obese patients after extubation, it is not rare that re-intubation and mechanical ventilator support is required [72]. As a result extubation should be performed on fully awake patients with sufficient reversal of neuromuscular block shown with monitoring, with cough and other protective reflexes fully returned, and before extubation aspiration with a gastric tube should definitely be performed [70,72]. In supine position reducing FRC may cause atelectasis, so it is recommended that the head be raised by 30-45 degrees before extubation [73]. Regaining pulmonary functions reduced during operations on obese patients may take 7-10 days, as a result CPAP or BIPAP administration may be given in the recovery period [72]. Sugammadex, used in recent years to reverse neuromuscular block before extubation, has been shown to reduce residual block by a significant degree compared to neostigmine [74]. In the postoperative period, the contribution of sufficient analgesia and chest physiotherapy administration to recovery of respiratory functions is great for obese patients [73,74].

IV. Laparoscopic Procedures in Obese Patients

Laparoscopy is visualization of the abdominal cavity with an endoscope. Carbon dioxide is the most commonly used insufflation gas for this procedure. Various pathophysiological changes are observed with carbon dioxide pneumoperitoneum and different patient positions. Full understanding of pathophysiological changes is necessary for an optimal anesthetic care. Today many surgical procedures are safely and efficiently applied with laparoscopic. Laparoscopic procedures offer numerous advantages including less postoperative pain, pneumonia and wound site infection, better respiratory functions and cosmetic appearance, shorter duration of recovery and discharge and lower total cost. The most common complaints following laparoscopic surgical intervention are pain, nausea and vomiting. However, these complaints are less severe compared to the similar open surgical interventions. With the introduction of laparoscopic bariatric surgery in 1994, this surgical method has attracted attention worldwide and become a part of daily procedures in a number of centers. [75]. Anesthetists should know well effects of laparoscopy in obese patient for perioperative management of these patients. 

a. Effects of CO2 pneumoperitoneum in obese patients:

Normally, CO2 absorved from the peritoneum is excreted from the lungs, but hypercapnia and acidosis may develop if intraoperative ventilation is distrupted [76]. Hypercapnia may cause stimulation of autonomic nervous system, cardiac arrhythmias, tachycardia and vasoconstriction in the pulmonary vessels. Acidosis has depressant effect on myocardial contractility. End-tidal CO2 (ETCO2 ) or partial CO2 pressure (PaCO2 ) should be closely monitored in order to prevent hypercapnia. ETCO2 value is usually lower than PaCO2 . 3 In a study with patients undergoing laparoscopic bariatric surgery, ETCO2 values were increased by 14% (from 35 to 40 mmHg), while PaCO2 values showed an increase by 10% (from 38 to 42 mm Hg) compared to the baseline values during laparoscopy [77]. Although both values were increased, normocapnia was achieved owing to proper ventilator adjustments. Adjustments in ventilation are necessary in order to prevent hypercapnia and acidosis during must be adjusted pneumoperitoneum. Dumont et al. reported that, minute ventilation should be increased by 21% in order to limit the increase of ETCO2 during gastroplasty [78].

 b. Effects of increased intraabdominal pressure during pneumoperitoneum:

As in non-obese persons, intraabdominal pressure is set at 15 mm Hg also in obese patients in order to provide adequate view and site. Intraabdominal pressure is 5 mmHg in non-obese individuals, while it is chronically elevated to 9-10 mm Hg in obese persons [79]. In a study with morbid obese people, heart rate and mean arterial pressure remained high both with open and laparoscopic gastric bypass surgery [80]. In addition, systemic vascular resistance, mean central pulmonary artery pressure and central venous pressure were increased, but pulmonary artery wedge pressure was not changed in obese patients. It has been shown in another study comparing obese and non-obese persons that, heart rate was increased by pneumoperitoneum in both groups, although this increase was more remarkable in obese patients. It has been reported in the same study that, cardiac outflow was increased by 12% following abdominal insufflation in morbidly obese patients [79,80]. In a study using Swan-Ganz catheterization, cardiac outflow has been reported to be decreased by 6% and stroke volume by 8% after abdominal [80]. Obese patients might be thought to better tolerate pneumoperitoneum since unlike non-obese patients, they are constantly exposed to high intra-abdominal pressure (9-10 mmHg) [81]. Hypovolemia reduces the preload, decreasing cardiac outflow. Therefore, absence of preoperative fluid deficit is important to minimize decreased venous return to the heart caused by pneumoperitoneum. Increased intraabdominal pressure during pneumoperitoneum pushes the diaphragm in a cephalic direction, resulting in increased pleural pressure which is also reflected on the cardiac cavities. Therefore, cardiac filling pressures may be measured incorrectly high. Increased intraabdominal pressure, reverse Trendelenburg position and hypercarbia may affect cardiac functions during laparoscopy [82]. Among these, hypercarbia can be prevented by proper ventilation. An arterial carbon dioxide pressure (PaCO2 ) under 45 mmHg does not affect cardiac functions. Increased intraabdominal pressure is recognized as the main reason for cardiac depression. Furthermore, reverse Trendelenburg position is not always a major determinant for hemodynamic condition [81,82]. Increased intraabdominal pressure blocks venous return, decreases preload, increases after load and causes reduction in cardiac flow [14]. These temporary disturbances return to normal after about 2-2.5 hours [83]. 

c. Effects of pneumoperitoneum on portal blood flow and postoperative changes in liver enzymes:

It has been shown in animal experiments and human trials that raising intraabdominal pressure to 15 mmHg decreases portal vein flow, alkaline phosphatase, albumin and total bilirubin and decreases aspartate transferase [82,83]. On the other hand, portal hypoperfusion may cause temporary increases in liver enzymes. Liver enzymes have been show to return to normal levels within 72 hours after laparoscopic cholecystectomy [80-83]. Transaminase values in morbid obese patients have increased by 6 folds after laparoscopic gastric bypass surgery, peaked at postoperative 24th hour and returned to baseline values at the 3rd day. Therefore, pneumoperitoneum is considered safe in obese persons with normal hepatic functions[84].

d. Effects of pneumoperitoneum on respiratory mechanics

Pneumoperitoneum has been shown to decrease respiratory compliance, increase airway pressure, respiratory rate, minute ventilation and reduce Tidal volume (increased peak inspiratory pressure) in non-obese patients. Similar condition applies for obese patients. Pulmonary compliance has been demonstrated to decrease by 31% in laparoscopic gastroplasty [83-85].In the same study, airway pressure also showed an increase by 17%. Pneumoperitoneum does not affect the gas exchange in obsere as in non-obese patients. No change occurred in physiologic dead space/ tidal volume ratio or alveolar-arterial oxygen gradient in morbid obese patients undergoing laparoscopic gastric bypass surgery [85]. 

e. Effects of laparoscopy on renal functions

Oliguria is seen during laparoscopy because of high intraabdominal pressure. There are a number of mechanisms reducing the amount of urine during laparoscopy: a. Kidney perfusion is reduced by the direct pressure effect on renal cortical blood flow. b. Renal blood flow is reduced by the direct pressure effect on the renal vessels. c. It cause increase in antidiuretic hormone, plasma renin activity and aldosterone levels. Keeping pneumoperitoneum at about 15 mmHg is thought to be safe is spite of intraoperative oliguria. No significant changes were observed in blood urea nitrogen and serum creatinine levels following laparoscopic gastric bypass surgery in morbidly obese patients. On the other hand, antidiuretic hormone, aldosterone and plasma renin activity [83-85].

f. Venous stasis:

Intraabdominal pressure and reverse Trendelenburg position have been shown to reduce femoral venous flow during laparoscopy. It has been demonstrated in a study conducted on obese patients that, the increased intraabdominal pressure reduced femoral systolic flow velocity by 43% and increased femoral sectional area by 52% during laparoscopic gastric bypass surgery. A combination of intermittent compression devices and antithrombotics may be needed in the prophylaxis deep vein thrombosis in morbid obese patients [82-86].


Obesity causes major changes in pulmonary mechanics. Compliance decreases, while elastance increases, FRC decreases and predisposition to shunt and hypoxemia increases. Adding effects of laparoscopy on this, peroperative ventilation management becomes more important. Patients undergoing laparoscopic bariatric surgery are at increased risk for hypoxemia, atelectasis, postoperative pneumonia and respiratory failure [87] .Obese patients often have accompanying comorbidities such as airway hyperreactivity, sleep apnea syndrome, obesity hypoventilation syndrome and pulmonary hypertension. Numerous studies have been conducted to determine the best ventilation strategy in obese patients. There is no difference between PCV and VCV in terms of better clinical outcome [85-87]. PCV-VG has theoretical advantages, because guarantees ensure minimal tidal volume at lower peak inspiratory pressure. In a study comparing VCV, PCV and PCV-VG modes in laparoscopic bariatric surgery, lower PIP was observed in PCV and PCV-VG compared to VCV mode, although no significant difference was found among these modes in terms of oxygenation or ventilation [88]. VT should be adjusted according to body weight in obese patients, because it is the thoracic garry tissue volume which is increased and not the lung volume. Keeping airway plateau pressure ≤ 30 cm H2 O may be difficult due to decreased airway compliance. It has been proposed that obese patient can tolerate higher inflation pressure, because intrathoracic fatty tissue limit over-distension of the lung in these patients [84-88]. Obese patients are prone to atelectasis. Many studies have shown that recruitment maneuver (RM) and PEEP application in obese patients imporove oxygenation and pulmonary mechanics. In their meta-analysis, Aldenkortt et al. concluded that recruitment maneuvers and PEEP do not pose risk for hypotension while improving oxygenation and pulmonary compliance In another meta-analysis, PEEP together with open lung approach improves postoperative oxygenation and decrease postoperative atelectasis [88,89]. Effects of recruitment maneuvers and PEEP ob postoperative oxygenation and pulmonary fucntions are controversial. Talab et al. reported that, 10 cm H2 O PEEP application following RM decreased atelectasis, improved intra- and postoperative oxygenation and shortened the length of stay in PACU [89]. In another study, Whalen et al. demonstrated that RM followed by 12 cm H2 O PEEP increased intraoperative oxygenation, but this effect disappeared 30 minutes after extubation. Ongoing studies such as PROBESE may find an answer to this question. There is no consensus on ideal oxygen concentration. Because high oxygen concentrations may cause absorption atelectasis, some authors suggest to keep the inspired oxygen concentration under 80 % [89]. However, in a meta-analysis by Hovaguimian et al. no concrete evidence was found for this suggestion. Finaly, recommendations for ventilation of obese patients include 6-8 ml/kg TV, PCV-VG mode, titration of respiratory rate according to normocapnia, lowering oxygen so as to provide SpO2 > 90, 10-15 cm H2 O, optimal PEEP, PIP or Ppl< 30 cm H2 O [85-89]. 

V. Management Of Postoperative Complications And Intensive Care In Obese Patients.

More than half of patients admitted to intensive care unit have a BMI higher than 25 kg/m2 . Many problems are encountered in obese patients admitted to intensive care unit, especially pulmonary and cardiovascular problems. With the increasing prevalence of obesity, rate of obese patients that will undergo any surgical operation has been increased. Therefore, rate of obese patients hospitakized and treated in intensive care unit has been increases in parallel. In a study by Sakr et al., among the patients admitted to intensive care units accross Europe, 3% have been reported as morbid obese, 15% obese and 36% overweight [90]. In addition, in a study by Lewandowski et al., rate of obese patients has been reported as about 20% of all patients admitted to intensive care unit. Although obesity is thought to be associated with increased rate of mortality in many aspects in preoperative, intraoperative and postoperative periods, yet there is no consensus in the literature on this association. Postoperative complications developing in obese patients increase the length of stay in hospital, resulting in increased costs [88, 89]. 

a. Airway and Respiration:

Providing airway in obese patients can make intubation and especially ventilation by mask difficult because of the anatomic changes. Therefore, measures should be taken for difficult intubation and ventilation in intensive care unit (ICU) and preparations for awake fibreoptic intubation should be made, when necessary [90]. Obese patients often develop arterial hypoxemia and ventilation-perfusion imbalance in supine position, and postoperative atelectasis. In order to avoid this, these patients should be taken to reverse Trendelenburg position and efforts should be made to prevent ventilation-perfusion imbalance, atelectasis and hypoxemia by decreasing the intrathoracic pressure. In addition, there is often a restrictive type respiratory pattern in obese patients because of the increased pressure against chest wall and displacement of the diaphragm upwards. Because of the increased risk of pneumonia in obese patients; respiratory physiotherapy, cold vapour, effective postoperative analgesia and early mobilization are recommended in the postoperative period. Additional measures should be taken in the postoperative period in these patients with close monitoring of respiration, and if deemed necessary with imaging modalities, pulse oximetry monitoring and arterial blood gas (ABG), because obesity has negative impacts on pulmonary functions [89-91]. Obese patients are at increased risk for venous thromboembolism (VTE) and pulmonary embolism because of increased plasminogen activator inhibitor (PAI-1), decreased capacity of tPA release from the endothelium, venous stasis, increased viscosity, increased fibrinogen and the presence of pulmonary hypertension.

b. Cardiac complications:

Postoperative cardiac complications in obese patients usually include hypertension, arrhythmia and myocardial infarction. Risk of heart failure is increased in the presence of hypertension. Atrial fibrillation (AF) is the most common form of cardiac arrhythmias. Occurrence of atrial fibrillation increases postoperative morbidity and mortality [92]. It has been reported in a study by Doyle et al. that, obesity causes disruption in diastolic functions as a results of the changes in the structure of atrium and ventricle and poses a risk for ventricular and atrial fibrillation [93]. However, in a study by Wanahita et al., AF has been found to be increased in obese patients compared to general population, but this did not increase the risk for AF after cardiac surgery [91, 92]. 

c. Infection:

Surgical site and intensive care induced infections are seen commonly in obese patients. Surgical site infection is the most important factor of morbidity and directly associated with the length of stay in hospital [93]. In a retrospective study by Karunakar et al. with 169 patients, increased BMI has been reported to increase the risk for wound site infection [94]. Surgical site infections should be avoided in obese patients by close monitoring of blood glucose, being vigilant for postoperative surgical site infection with insulin and antibiotic therapy if deemed necessary, postoperative oxygen administration, proper wound care, pain control and providing sufficient antibiotic concentration in the tissues [95].

d. Other complications:

Necessary measures should be taken in the postoperative period in obese patients for renal failure risk, multiple organ failure risk, catheter related complications (during insertion and use) and, occurrence of decubitus ulcers or peripheral nerve injury at the relevant pressure points related to the position in the intra- and postoperative periods.Comparing with non-obese patients, obese patients followed-up in intensive care unit have following characteristics: higher blood glucose values (increased stress response), lower growth hormone levels, higher insulin levels and increased cortisol, noradrenalin and adrenalin levels. In addition, keton and free fatty acid levels are also higher. Resting energy expenditure is normal in intensive care unit with high muscle and nitrogen loss [96]. Despite much fat deposition, protein-calorie malnutrition may develop very quckly in morbidly onese patients. This is because increased basal insulin level to suppress lipid mobilization, and meet energy requirement by breaking down proteins and stimulating gluconeogenesis. Protein degradation in obese patients hospitalized in intensive care unit is higher by 50% than non-obese patients. The main question about nutrition of obese patients in ICU is whether hypocaloric nutrition which would meet protein requirement, but provide less calories than consumed is proper or not. Society of Critical Care medicine (SCCM) and American Society for Parental and Enteral Nutrition (A.S.P.E.N) guidelines state that hypocaloric nutrition in obese patients protects the nitrogen balance and decrease morbidity. However, sample size is small in the used publications and presence of kidney or liver disease has not been evaluated in these patients and also its impact is poor on survival. Hypocaloric nutrition decreases the length of stay in intensive care unit and the number of days spent on mechanical ventilation, although this was not proven scientifically [97,98].

Considering all factors, risk of mortality is increased by 1.2 folds in overweight and 1.5 folds in obese persons compared to normal weight people [98]. In contrary, obesity has been found to have a protective effect in intensive care patients and to be associated with low rate of mortality. This is defiend as ‘obesity paradox’ and emphasized in prospective studies. In their prospective study with 493 intensive care patients, Peake et al. reported that middle and long term mortality was decreased with the increase in BMI which was thought to have potential positive effect on survival [99]. Whereas other studies conducted have reported that obesity has no effect on mortality; however, it prolongs the length of stay in intensive care unit and hospital [96-100]. In another meta-analysis, no difference has been found in intensive care unit mortality, although hospital mortality was lower among obese and morbid obese patients. No correlation has been found between obesity and the lngth of stay in hospital and duration of mechanical ventilation [101]. Paolini et al. have reported that rate of mortality was high (44%) in obese patients with abdominal adiposity and high abdominal diameter was a more independent risk factor than high BMI.There is not a full consensus on treatments, procedures to be performed and expected outcome of these procedures in obese patients followed-up in intensive care unit due to any reason. Therefore, individualized and targeted planning should be made for each patient [101, 102]. In conclusion; obesity which becomes increasingly widespread and one of the most important health problems in the world is a preventable and treatable disease and health problem. Obesity significantly influences quality and length of life and its treatment requires advanced level of specialty and experience. Advancement in technology is continuously expanding the boundaries of laparoscopic surgery, bringing new risks besides advantages. Successful anesthesia management in laparoscopic interventions, co-ordinated team work with many disciplines and well-designed types of care. In terms of achieving the best results and reducing complications, it is difficult to cope with altered physiology in such patients. Anesthesiologists should deliver an anesthesia management considering the factors that would minimize these risks.


1. Sturm R. Increases in morbid obesity in the USA: 2000- 2005. Public Health . 2007, 121(7): 492-496.

2. Arslan M, Turgut H. C. Physiological Changes and Pharmacocinetics in Obesitiy. J Anest Reanim-Special Topics. 2015, 8(2): 1-10.

3. World Health Organization. Obesity and overweight. Fact Sheet. 2006,31.

4. Forbes GB, Welle SL. Lean body mass in obesity. Int J Obes. 1983, 7(2): 99-107.

5. JP Adams, PG Murphy. Obesity in anaesthesia and intensive care. Br J Anaesthesia. 2000, 85(1): 91-108.

6. Blouin RA, Warren GW. Pharmacokinetic considerationsin obesity. J Pharm Sci. 1999, 88(1): 1-7.

7. Feng B, LaPerle JL, Chang G, Varma MV. Renal clearance in drug discovery and development: molecular descriptors, drug transporters and disease state. Expert Opin DrugMetab Toxicol. 2010, 6(8): 939-952.

8. Jansson PA, Larsson A, Lonnroth PN. Relationshipbetween blood pressure, metabolic variables and blood flow in obese subjects with or without non-insulin-dependent diabetesmellitus. Eur J Clin Invest. 1998, 28(10): 813-818.

9. Griffin KA, Kramer H, Bidani AK. Adverserenal consequences of obesity. Am J Physiol Renal Physiol. 2008, 294(4): F685-696.

10. VE Ortiz , J Kwo. Obesity: physiologic changes and implications for preoperative management. BMC Anesthesiology . 2015, 15: 97.

11. CM Salome, GG King, NBerend. Pulmonary Physiology and Pathophysiology in Obesity. J Appl Physiol. 2010, 108: 206–211.

12. Cullen A, Ferguson A. Perioperative management of the severely obese patient: a selective pathophysiological. Can J Anaesth. 2012, 59(10): 974-996.

13. Ogunnaike BO, Whitten CW. Anesthesia and obesity. In: Barash PG, Cullen BF, Stoelting RK, eds. Clinical Anesthesia. Philadelphia, PA: Lippincolt Williams&Wilkins. 2006, 1040- 1052.

14. Domi R, Laho H. Anesthetic challenges in the obese patient. J Anesth . 2012, 26(5): 758-765.

15. Ingrande J, Lemmens HJ. Dose adjustment of anaesthetics in the morbidly obese. Br J Anaesth . 2010, 105 (Suppl 1): 16-23.

16. Patil SP, Schneider H, Schwartz AR, Smith PL. Adult obstructive sleep apnea. Chest. 2007, 132(1): 325-337.

17. Hillman DR, Loadsman JA, Platt PR, Eastwood P. Obstructive sleep apnea and anaesthesia. Sleep Med Rev. 2004, 8(6): 459-71.

18. Ogunnaike BO, Jones SB, Jones DB, Provost D, Whitten CW. Anesthetic considerations for bariatric surgery. Anesth Analg. 2002, 95(6): 1793-805.

19. Apfelbaum JL, Hagberg CA, Caplan RA, Blitt CD, Connis RT et al. American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Practice guidelines for management of the difficult airway: an updated report by the American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Anesthesiology. 2013, 118(2): 251-270.

20. Forbes GB, Welle SL. Lean body mass in obesity. Int J Obes. 1983, 7(2): 99-107.

21. Jansson PA, Larsson A, Lonnroth PN. Relationship between blood pressure, metabolic variables and blood flow in obese subjects with or without non-insulin-dependent diabetesmellitus. Eur J Clin Invest. 1998, 28(10): 813-818.

22. Yusuf S, Hawken S, Ounpuu S, Bautista L, Franzosi MG et al. INTERHEART Study Investigators. Obesity and the risk of myocardial infarction in 27000 participants from 52 countries: a case-control study.Lancet. 2005, 366(9497):1640- 1649.

23. Lavie CJ, Milani RV, Ventura HO, Romero- Corral A. Body composition and heart failure prevalence and prognosis: getting to the fat of the matter in the ‘‘obesity paradox’’. Mayo Clin Proc. 2010, 85(7): 605-608.

24. Wall RT. Endocrine disease. In: Hnes RL, Marschall KE, eds. Stoelting’s Anesthesia and Co-existing Disease. 5th ed. Philadelphia , PA: Churchill Lilingstone. 2008, 365-406.

25. D Ismail, BAYAR M K. Preoperative and Comorbid Diseases in Obese Patients. J Anest Reanim-Special Topics. 2015, 8(2): 11-7.

26. Benumof JL. Obesity, sleep apnea, the airway, and anesthesia. Curr Opin Anes. 2004, 17(1): 21-30.

27. Kaneko Y, Floras JS, Usui K, et al. Cardiovaskular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N. Engl. J Med. 2003, 348(13): 1233-1241.

28. Kristensen MS. Airway management and morbid obesity. Eur J Anaesthesiol. 2010, 27(11): 923-927.

29. Wadhwa A, Singh PM, Sinha AC. Airway management in patients with morbid obesity. Int Anesthesiol Clin. 2013, 51(3): 26-40.

30. Center for Disease Control and Prevention. Vital signs: Obesity prevelance among adults-United States 2009. MMWR Morb Mortal Wkly Rep. 2010, 59: 951-955.

31. Brodsky JB, LemmensHJM, Brock-Utne JG, et al. Morbid obesity and tracheal intubation . anesth Analg. 2002, 94(3): 732-736.

32. Buckley FP, Robinson NB, Simonowitz DA, et al. Anesthesia in the morbidiy obese: a comparison of anaesthetic and analgesic regimens for upper abdominal surgery. Anaesthesia. 1983, 38 (9): 840-851.

33. Mondolfi RN, JonesTM, Hyre AD, et al. Comparison of percent of United States adults weighing > or-300 pounds (136 kilograms) in three time periods and comparison of five atherosclerotic risk factors for those weighing > or =300 ponuds to those < 300 pounds. Am J Cardiol. 2007, 100(11): 1651- 1653.

34. Sapala JA, Wood MH, Schuhknecht MP, et al. Fatal pulmonary embolism after bariatric operations for morbid obesity. A 24 –year retrospective analysis. Obes surg. 2003,13(6): 819-825.

35. Salihoglu Z, Demiroluk S, Dikmen Y. Respiratory mechanics in morbid obese patients with chronic obstructive pulmonary disease and hypertension during pneumoperitoneum. Eur J Anaesthesiol. 2003, 20(8): 658-661.

36. Hsieh CH. Laparoscopic cholecystectomy for patients with chronic obstructive pulmonary disease. J Laparoendosc Adv Surg Tech A. 2003, 13(1): 5-9.

37. Nishiyama T, Kohno Y, Koishi K. Anesthesia for bariatric surgery. Obes Surg. 2012, 22: 213-219.

38. Jayaraman L, Sinha A, Punhani D. A comparative study to evaluate the effect of intranasal dexmedetomidine versus oral alprazolam as a premedication agent in morbidly obese patients undergoing bariatric surgery. J Anaesthesiol Clin Pharmacol 2013; 29(2): 179-182.

39. Ogunnaike BO, Whitten CW. Anesthetic management of morbidly pbese patients. Seminars in Anesthesia, Perioperative Med Pain. 2002, 21(1): 46-58.

40. Lebuffe G, Andrieu G, Wierre F, Gorski K, Sanders V et al. Anesthesia in the obese. J Visc Surg. 2010, 147S: e11-e19.

41. Atak F, Is?k B. General anesthesia in obese patients. Turkiye Klinikleri J Anest Reanim- Special Topics. 2015, 8: 18-23.

42. Ogunnaike BO, Jones SB, Jones DB, Provost D, Whitten CW. Anesthetic considerations for bariatric surgery. Anesth Analg. 2002, 95(6): 1793-805.

43. Leykin Y, Miotto L, Pellis T. Pharmacokinetic considerations in the obese. Best Pract Res Clin Anaesth. 2011, 25(1): 27-36.

44. Nightingale CE, Margarson MP, Shearer E, Redman JW, Lucas DN et al. Perioperative management of the obese surgical patient 2015. Anaesthesia. 2015, 70: 859-76.

45. Ingrande J, Lemmens HJM. Dose adjustment of anaesthetics in the morbidly obese. British J Anesth. 2010, 105(S1): i16-i23.

46. Dixon BJ, Dixon JB, Carden JR. Preoxygenation is more effective in the 25 degrees head-up position than in the supine position in severely obese patients: a randomized controlled study. Aneshesiology. 2005, 102(6): 1110-1115.

47. Terkawi AS, Durieux ME. Perioperative anesthesia care for obese patients. Anesthesiology News. 2015, 1-12.

48. Warner MA, Warner ME, Martin JT. Ulnar neuropathy. Incidence, outcome, and risk factors in sedated or anesthetised patients. Anestheiology. 1994, 81(6): 1332-1340.

49. Sprung J, Whalley DG, Falcone T, Wilks W, Navratil JE et al. The effects of tidal volume and respiratory rate on oxygenation and respiratory mechanics during laparascopy in morbidly obese patients. Anesth Analg. 2003, 97(1): 268-274.

50. Oberg B, Poulsen TD. Obesity: An anaesthetic challenge. Acta Anaesthesiol Scand. 1996, 40(2): 191- 200.

51. Torres-Villalobos G, Kimura E, Mosqueda JL, GarciaGarcia E, Dominguez-Cherit G et al. Pressure-induced rhabdomyolysis after bariatric surgery. Obes Surg. 2003, 13(2): 297-301.

52. Bamgbade OA, Rutter TW, Nafiu OO, Dorje P. Postoperative complications in obese and nonobese patients. World J Surg. 2007, 31(3): 556-60.

53. Wittgrove AC, Clark GW, Tremblay LJ. Laparoscopic gastric bypass, Roux-en-Y: preliminary report of five cases. Obes Surg. 1994, 4(4): 353-357.

54. Lindgren L, Koivusalo AM, Kellokumpu I. Conventional pneumoperitoneum compared with abdominal wall lift for laparoscopic cholecystectomy. Br J Anaesth. 1995, 75(5): 567-572.

55. Sharma KC, Brandstetter RD, Brensilver JM, et al. Cardiopulmonary

56. Nguyen NT, Anderson J, Fleming NW, et al. Effects of pneumoperitoneum on intraoperative respiratory mechanics and gas exchange during

57. Dumont L, Mattys M, Mardirosoff C, et al. Changes in pulmonary mechanics during laparoscopic gastroplasty in the morbidly obese pa- tient. Acta Anaesthesiol Scand. 1997, 41(3): 408–413.