**2. Physiological changes**

According to the National Institutes of Health, a BMI >40 increases the risk for diabetes mellitus, cardiovascular disease, and reduced life expectancy [13]. Understanding the differences in anatomy and physiology of morbidly obese patients is critical for surgical planning.

#### **2.1 Cardiovascular**

Myocardial infarction, cardiac failure, and sudden cardiac death risk increase in obese individuals. This may be due to increased body mass leading to hemodynamic and cardiovascular changes resulting in increased cardiac output, larger stroke volume, decreased vascular resistance, and increased cardiac workload [14]. In autopsy studies comparing obese and non-obese patients it has been found that obese patients can have 20–55% larger cardiac diameters, hypertrophied ventricles, and increased cardiac weight. These changes in cardiac physiology can result in hypertension and ultimately lead to cardiac failure [15]. Studies have found that ventricular hypertrophy and cardiac failure caused by obesity results in a higher risk of mortality [16]. The eccentric and concentric ventricular hypertrophy associated with obesity can lead to prolonged Q-T intervals or tachyarrhythmia. Additionally, unexplained cardiac arrhythmias are more common in obese patients [11]. The creation of pneumoperitoneum required to perform minimally invasive procedures can cause further cardiac depression. Abdominal insufflation causes an increase in afterload while the subsequent impeding of a venous return causes a decrease in preload. This contributes to an overall reduction in cardiac output [17]. Cardiac depression during laparoscopic procedures is often transient as the patient's body compensates for the change in physiology. In one study of morbidly obese patients undergoing laparoscopic gastric bypass, cardiac output levels returned to baseline at 2.5 hours after abdominal insufflation [17].

### **2.2 Pulmonary**

Due to fat deposits in the mediastinum and abdominal cavities, the mechanical properties of the lungs and chest wall are altered in obese patients resulting in reduced compliance of the lungs, chest wall, and entire respiratory system. These changes likely contribute to increased symptoms of wheezing, dyspnea, and orthopnea [18]. Obesity causes reduced chest wall and pulmonary compliance and therefore reduction in gas exchange and increased bronchial resistance and ventilation-perfusion. Increased abdominal pressure and pleural pressures in obesity alter the breathing pattern resulting in a reduction of both expiratory reserve volume (ERV) and the functional residual capacity (FRC). Severely obese patients have a decreased FRC up to 33% [11, 18].

The expiratory reserve volume is also compromised by 35–60%, secondary to cephalad displacement of the diaphragm by the obese abdomen [19]. Sleepdisordered breathing, including obstructive sleep apnea (OSA) and obesity-related respiratory failure (ORRF) is common in obese patients. Studies demonstrated that half of all patients with a BMI >40 kg/m<sup>2</sup> demonstrate OSA [20]. Untreated OSA can result in hypoxemia during sleep as well as pulmonary hypertension, both of which increase risk of cardiac arrythmias. In addition, OSA has been associated with postoperative respiratory complications pneumonia, postoperative hypoxemia, and unplanned reintubation [11].

There are additional intrinsic qualities of an obese body habitus that can impair respiratory function. More soft tissue of the upper airway combined with increased tongue size can cause significant upper airway resistance [16]. An increase in breast mass and additional adiposity can cause difficulty with direct laryngoscopy [16]. Finally, a waist-to-hip ratio has been found to poorly impact gas exchange with larger waist-to-hip ratios correlating to worsening arterial blood gas values [11, 16, 21].

Performing a minimally invasive hysterectomy requires the patient to undergo general anesthesia, the creation of pneumoperitoneum, and supine positioning, all of which further impact respiratory physiology in obese patients. The administration of general anesthesia can reduce a patient's FRC by an additional 20%, while pneumoperitoneum increases inspiratory resistance requiring higher minute ventilation [11, 15]. In one study evaluating respiratory mechanics in laparoscopy, it was found that obese, anesthetized patients in the supine position required 15% higher minute ventilation to maintain normocarbia prior to abdominal insufflation. The authors also reported that these patients had 30% lower static compliance and 68% higher inspiratory resistance after insufflation of the abdomen with CO2 to a pressure of 20 mmHg [15, 22]. While the increase in inspiratory restitance caused by obesity requires higher minute ventilation, oxygenation does not seem to be affected by abdominal insufflation or Trendelenburg positioning. Therefore, patients who are able to tolerate general anesthesia in the supine position are likely also able to tolerate abdominal insufflation and changes in position including Trendelenburg [15, 22].

#### **2.3 Gastrointestinal system**

Gastric and esophageal function may also be impaired in obese patients, which can lead to intra-operative challenges. Gastroesophageal reflux disease (GERD) and hiatal hernias are found more commonly in obese patients and can often be asymptomatic [11]. This is caused by increased intra-abdominal pressure which can be two to three times higher in morbidly obese patients compared with non-obese patients [11]. Studies have found that obese patients tend to have higher gastric

volumes, lower gastric pH, and delayed emptying which can increase their risk of intra-operative and post-operative gastric acid aspiration [11, 15]. For this reason, a prophylactic H2 blocker (ranitidine) and a pro-kinetic (metoclopramide) are often recommended prior to a surgical procedure [16].

### **2.4 Thromboembolism**

Obesity is an independent risk factor for venous thromboembolism (VTE). Current data regarding the risk of VTE in gynecologic surgery shows the incidence of VTE in gyn surgery ranges from 0 to 2%. Evidence for these studies is from retrospective studies in non-obese patients who underwent simple laparoscopic procedures [11]. Gynecologic laparoscopic procedures with a duration of >30 min are considered moderate to high risk for VTE. Increasing laparscopic surgical complexity increases rates of VTE after completion of surgery according to the American College of Chest Physicians (ACCP) [23]. For these procedures, the standard treatment for VTE prophylaxis is mechanical prophylaxis with sequential compression devices. For obese patients it is critical these devices are appropriately fitted. Alternatively, pharmacologic prophylaxis with either subcutaneous low molecular weight heparin or unfractionated heparin can be administered. For bariatric surgery patients who have a BMI >55, immobility, history of active or recent VTE, hypercoagulable disorders, or severe OSA there are recommendations for placement of an inferior vena cava (IVC) filter for patients prior to bariatric surgery [24]. There are no current clear guidelines for patients undergoing gynecologic laparoscopic surgery and decisions should be made on an individual basis. The ACCP recommends dual prophylaxis with sequential compression devices and pharmacologic prophylaxis during admission and prolonged pharmacologic prophylaxis for 2–4 weeks after discharge for patients with gynecologic cancer with additional risk factors such as age >60 or history of VTE [23]. Recommendations for patients who are morbidly obese undergoing gynecologic laparoscopy may include combination mechanical and pharmacological prophylaxis during surgery and hospitalization. Taking into consideration patient comorbidities and mobility status, extended prophylaxis after discharge may also be considered [11].
