The risk of death from all causes increases throughout the range of moderate and severe overweight for both men and women in all age groups [4, 8]. The graphed relationship between body mass index (BMI) and mortality is “J-shaped” with increased death rates with malnutrition and with increasing BMI [4, 9]. Obesity is associated with an increased risk of death in hospitalized patients. The association between BMI and mortality is altered in the critically ill. Paradoxically, patients who are overweight (BMI 26–30; class I obesity) and moderately obese (BMI 30–40; class II obesity) have a lower mortality than patients of normal body weight [10, 11]. Meta-analyses have indicated that survival in obese ICU patients may be better or at least unchanged when compared to non-obese critically ill patients [12, 13]. In a recent Italian epidemiological cohort study the highest risk of death in the ICU was reported in underweight or morbidly obese patients, while overweight and obesity of class I/II were associated with a lower ICU mortality [14]. While some studies have suggested that morbidly obese patients (BMI >40) are at an increased risk of dying this observation has not been demonstrated by other studies [15]. Obesity is however associated with a prolonged duration of mechanical ventilation and increased ICU length of stay [12, 15]. The increased production of anti-inflammatory mediators by adipose tissue and the increased energy reserve has been postulated to account for the protective effect of moderate obesity during critical illness.

The effects of obesity on respiratory function are complex and influenced by the degree of obesity, age and body fat distribution (central or peripheral). The expiratory reserve volume (ERV) is consistently decreased in obese patients while the FEV1 to FVC ratio is increased [16]. The vital capacity (VC), total lung capacity (TLC) and functional residual volume (FRV) are generally maintained in otherwise normal individuals with mild to moderate obesity but are reduced by up to 30 % in morbidly obese patients.

Obese patients have an increased work of breathing due to abnormal chest elasticity, increased chest wall resistance, increased airway resistance (Raw), abnormal diaphragmatic position and upper airway resistance, as well as the need to eliminate a higher daily production of carbon dioxide. Patients with morbid obesity are generally hypoxemic, with a widened alveolar-arterial oxygen gradient caused by ventilation-perfusion mismatching The FRC falls when assuming a supine position, further increasing ventilation-perfusion mismatching. Abnormalities in the control of ventilation are common in obese patients with a high percentage of patients having obstructive sleep apnea and daytime hypoventilation. Patients with severe obesity (BMI generally greater than 40) may develop chronic hypoventilation with hypercapnic respiratory failure (MOHS). Presumably the increased work of breathing results in resetting of the respiratory control centers. Patients who present to the ICU with MOHS are best managed by non-invasive ventilation; mechanical ventilation may result in severe adverse sequelae in these patients (see Management of MOHS).

Particular attention to ventilator settings is required in obese patients who require mechanical ventilation. Lung volumes are determined by height and sex and not by weight. Lung volumes do not increase (grow) with increasing body weight. Tidal volumes MUST therefore be set according to ideal body weight and NOT actual body weight. Using actual body weight will result in severe barotrauma. The initial tidal volume should be based on IBW and adjusted according to inflation pressures and blood gases. In patients with chronic CO₂ retention, minute ventilation should be titrated to normalize pH and not pCO₂. Positive expiratory pressure (PEEP) is required to prevent end-expiratory airway closure and atelectasis. A PEEP of 8–10 cm H₂o is generally recommended. However in patients with severe obesity PEEP is best determined by measuring intrapleural pressures using an esophageal balloon (see Chaps. 19 and 23). We have previously reported a mean end-expiratory pressure of 17.0 ± 2.9 cm H₂O in patients with MOHS [11]. Bilevel/APRV may be a particularly useful mode of ventilation in the morbidly obese patient [17].

Weaning the obese patient from mechanical ventilation is frequently a difficult and challenging task. Burns and colleagues have demonstrated that in obese patients the reverse Trendelenburg position at 45° resulted in a larger tidal volume and lower respiratory rate than the 0, or 90° position, and they postulated that this position may facilitate the weaning process [18].

Obese patients are at particular risk for aspiration pneumonia, especially in the postoperative period. This risk is increased due to several factors, including a higher volume of gastric fluid, a lower than normal pH of gastric fluid in fasting obese patients, increased intra-abdominal pressure and a higher incidence of gastroesophageal reflux. This is another important reason to nurse the obese patient in the semi-upright position. Obesity is an important risk factor for pulmonary embolism. The high risk of thromboembolic disease in obese ICU patients, warrants an aggressive approach to deep venous thrombosis prophylaxis.

Endotracheal intubation can be a challenging in the morbidly obese patient. In the Australian Incident Monitoring Study, obesity with limited neck mobility and mouth opening accounted for the majority of cases of difficult intubation [19]. Physicians caring for these patients must be well versed in intubation techniques as well as the use of adjuncts for intubation.

The alterations of cardiac function in patients with severe obesity are complex due to the frequent presence of comorbid conditions including systemic hypertension, diabetes, and hyperlipidemia [20]. Patients with morbid obesity have an increase in total blood volume and resting cardiac output. Both increase in direct proportion to the amount the patient weighs over the IBW. The cardiac index and stroke index are normal in otherwise healthy obese patients. Obesity is an independent risk factor for left ventricular hypertrophy [21–24]. Left ventricular hypertrophy is related to the increased cardiac output associated with obesity as well as the effect of adipokines (leptin, adiponectin, cardiotrophin-1) on myocyte function [24–26]. Left ventricular hypertrophy results in an increased incidence of diastolic dysfunction. Although the resting cardiac output is increased, obese patients have been demonstrated to have impaired left ventricular contractility and a depressed ejection fraction.

The left ventricular filling pressure is elevated in obese patients due to the combination of increased preload and reduced ventricular distensibility. Consequently, fluid loading is poorly tolerated in these patients.

Obesity is associated with fatty infiltration of the liver. This may be asymptomatic or result in non-alcoholic steatohepatitis (NASH) and cirrhosis. NASH may be evident by increased transaminases, increased NH3 and increased serum ferritin and triglyceride concentrations [27, 28]. Chronic renal insufficiency is common in patients with obesity. This is related to the increased incidence of hypertension and diabetes; however obesity is associated with a focal segmental glomerulosclerosis which is known as obesity-related glomerulopathy [29, 30].

Drug distribution, metabolism, protein binding, and clearance is altered by the physiological changes associated with excessive weight Some of these pharmacokinetic changes may, however, negate the consequences of others and the pharmacokinetic alterations may differ in the morbidly obese compared to the mildly or moderately obese. However, a number of drugs used in the ICU, most notably digoxin, aminoglycosides and cyclosporin, can cause drug toxicity if the obese patients are dosed based on their actual body weight.

In obese patients with renal dysfunction, the creatinine clearance, as calculated using standard formulae, correlates very poorly with the measured creatinine clearance [31]. Therefore, in the obese patient with renal dysfunction, the dosing regimen of renally excreted drugs should be based on the measured creatinine clearance [32].

Nutrition should not be withheld from the obese patients in the mistaken belief that weight reduction is beneficial during critical illness. Sarcopenia is the loss of lean body mass (muscle mass) that occurs with aging. Sarcopenic obesity is a body composition category in which obesity is accompanied by low skeletal muscle mass [33]. In Western societies, the age group of the population with the highest prevalence of obesity ranges from 55 and 75 years [34, 35]. Sarcopenic obesity is therefore especially prevalent in the elderly [36]. Patients with sarcopenic obesity are likely to develop severe protein energy malnutrition in response to metabolic stress.

Obese patients should generally receive between 20 and 25 Kcal/Kg of IBW/ day (see Chap. 32). Most of the calories should be given as carbohydrates with fats given to prevent essential fatty acid deficiency. It has been suggested that critically ill obese patients receive nutritional support with a hypocaloric high-protein formulation [37, 38]. It has been postulated that if adequate protein is supplied and obligatory glucose requirements are met, endogenous fat stores will be used for energy [39]. Current consensus recommends a level of 1.5–2.0 g/kg of IBW to achieve nitrogen equilibrium [40].

One of the most challenging features of the morbidly obese patient is venous and arterial access. Poor peripheral venous sites in these patients necessitate more frequent use of central venous access. A short stubby neck, loss of physical landmarks and a greater skin-blood vessel distance make internal-jugular and subclavian vein cannulation technically difficult.

Obese patients have a higher incidence of catheter malpositions and local puncture complications, with catheter related infections and thromboses. Femoral venous access may not be possible as these patients usually have severe intertrigo and morbid obesity is a major risk factor for catheter associated blood stream infection (CRBI) when the femoral site is used [41]. The use of Doppler ultrasound-guided techniques for obtaining central venous access is recommended in these patients. Furthermore, early placement of a PICC should be considered.

Bedside radiographs are of a very poor quality in the morbidly obese patient, limiting their diagnostic value. Abdominal and pelvic ultrasonography is limited by extensive abdominal wall and intra-abdominal fat. Percutaneous aspiration and drainage of intraperitoneal and retroperitoneal collections may be hindered by the obese body habitus. Many computed tomography tables have weight restrictions (about 350 lbs.) that prohibit imaging of morbidly obese patient.

MOHS is a systemic illness involving many organ systems related to extreme obesity [7]. The organ systems associated with MOHS include hypercapnic respiratory failure, systemic hypertension, left ventricular hypertrophy with diastolic dysfunction, pulmonary hypertension, right ventricular volume overload, chronic renal insufficiency and NASH. The pathophysiology of MOHS is related to the complex interactions and feed-back loops. The defining feature of MOHS is chronic hypercapnic respiratory failure. Lung function tests in demonstrate a restrictive pattern. Remarkably, however the majority of these patients have been diagnosed and treated for chronic obstructive lung disease. The diagnostic features of MOHs are listed below¹: