The high risk of thromboembolic disease in obese patients in intensive care justifies an aggressive approach towards the prevention of deep vein thrombosis. Low molecular weight heparin (LMWH), oral anticoagulation, or the combination of pneumatic compression and LMWH should be considered in the morbidly obese patient in intensive care. Deep vein thrombosis (DVT) is complicated by the fact that pneumatic compression devices are often poorly tolerated by the morbidly obese patient. In those patients in whom anticoagulation is contraindicated, prophylactic placement of a filter in the inferior vena cava should be considered (Meilahn et al., 1996). Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an Original Essay Endotracheal intubation can be a daunting experience for the morbidly obese patient and probably the intensivist's worst nightmare. In the Australian Incident Monitoring Study, obesity with limited neck mobility and mouth opening accounted for the majority of cases of difficult intubation. In obese patients, endotracheal intubation should not be attempted by an inexperienced physician and equipment for urgent airway management (including surgical airway instruments) should be readily available (Williamson et al., 1993). Management Considerations in Cardiac Patients Admitted to the Intensive Care Unit Morbid obesity is characterized by increased total blood volume and resting cardiac output. Both increase in direct proportion to the patient's weight compared to ideal body weight (IBW). The increase in cardiac output is related exclusively to an increase in stroke volume, while heart rate remains unchanged. Cardiac index and stroke index are normal in otherwise healthy obese patients (Rexrode KM et al., 1996). The increase in cardiac output is accompanied by a decrease in systemic vascular resistance in normotensive patients. De Divitiis and colleagues performed left and right heart catheterization in 10 morbidly obese (mean BMI of 48.8) but otherwise healthy individuals. These authors noted that mean oxygen consumption (VO) was increased (311 mL/min) and that VO increased linearly with increasing body weight. The arteriovenous oxygen difference was however normal, suggesting that cardiac output increases primarily to meet the metabolic demands of excess fat (De Divitiis et al., 1983). It has been reported that the distribution of cardiac output is similar in obese and lean individuals. Although resting cardiac output is increased, obese patients have been shown to have reduced left ventricular contractility and reduced ejection fraction, both at rest and after exercise. Decreased myocardial p-adrenergic receptors may contribute to this finding (Rexrode KM et al., 1996). Additionally, left ventricular mass, left ventricular wall thickness, and left ventricular cavity size may increase, resulting in left ventricular dilatation and hypertrophy. These changes are related to the degree and duration of obesity (Berkalp B et al., 1995). Systemic arterial hypertension is common in morbidly obese patients, with superimposed left ventricular hypertrophy. It should be noted that the use of standard sized sphygmomanometry cuffs will result in inaccurate blood pressure recordings and therefore appropriately sized cuffs should be used. Diastolic dysfunction with a prolonged relaxation phase and abnormalities ofEarly filling is an early indicator of cardiac involvement in obesity (Berkalp B et al., 1995). Electrocardiographic changes associated with obesity include a leftward shift of the QRS axis and an increase in PR, QRS, and QTc intervals. In general, left ventricular filling pressure is elevated in obese patients due to the combination of increased preload and reduced ventricular distensibility (Backman L et al., 1983). In general, left ventricular filling pressure is elevated in obese patients due to a combination of increased preload and reduced ventricular distensibility. De Divitiis and colleagues reported a mean left ventricular end-diastolic pressure (LVEDP) of 16.6 mm Hg in their series of patients. Consequently, fluid loading is poorly tolerated by the obese patient (De Divitiis et al., 1983). Drug dosing considerations in critically ill obese patients. The distribution, metabolism, protein binding, and clearance of many drugs are altered by the physiological changes associated with obesity (Abemethy & Greenblatt, 1982). Some of these pharmacokinetic changes may, however, override the consequences of others, and the pharmacokinetic alterations may differ in the morbidly obese individual compared to the mildly or moderately obese individual. Furthermore, the patient's underlying disease can substantially influence the pharmacokinetic properties of a drug. Therefore, the net pharmacological alteration in any patient is often uncertain. However, for a number of drugs used in intensive care, particularly digoxin, aminophylline, aminoglycosides, and cyclosporine, drug toxicity may occur if patients are dosed based on their actual body weight. Oral absorption of drugs remains substantially unchanged in obese patients. The volume of distribution (Vd) of drugs in obese patients largely depends on the lipophilicity of the drug (Blouin et al., 1987). The Vd of weakly lipophilic drugs (aminoglycosides, quinolones) is moderately increased compared to that of weakly lipophilic drugs (aminoglycosides, quinolones). situation in normal individuals, but the Vd corrected by actual body weight is significantly lower. Vd is increased for many, but not all, lipophilic drugs. The clearance of most hepatically metabolised drugs is not reduced. For drugs excreted renally, elimination will depend on creatinine clearance. A higher glomerular filtration rate has been reported in obese patients with normal renal function, and this rate will increase the clearance of drugs that are eliminated primarily through glomerular filtration (Blouin et al., 1982). In obese patients with renal dysfunction, creatinine clearance, as calculated using standard formulas, correlates very poorly with measured creatinine clearance. In the obese patient with renal dysfunction, the dosing regimen of renally excreted drugs should be based on measured creatinine clearance (Blouin et al., 1987). As a result of the complexity of pharmacokinetic changes that can occur in obese patients and the limited data available for many drugs, there is inconsistency and disagreement in the literature regarding drug dosing in obesity (Blouin et al., 1987). For many medications, it is unclear whether dosage adjustments should be made based on weight and whether such adjustments should be based on actual body weight, IBW, or a percentage of actual body weight. Dosing recommendations for medications commonly used in intensive care are listed in Table 3 below (Abemethy & Greenblatt, 1982). Due to limited data andsometimes conflicting on which these recommendations are based, monitoring of clinical endpoints, signs of toxicity, clinical response, and serum drug levels (when available) is essential (Abemethy & Greenblatt, 1982). Obtaining adequate venous access in another serious problem in the critically ill obese patient in intensive care. Inadequate peripheral venous sites in obese patients require more frequent use of central venous access. A short, stocky neck, loss of physical landmarks, and increased distance between the skin and blood vessels make internal jugular and subclavian vein cannulation technically difficult (Boulanger et al., 1994); this difficulty translates into a greater incidence of catheter malpositioning and local puncture complications. Increased numbers of skin punctures during catheter insertion and delayed catheter changes may lead to more catheter-related infections and thrombosis (Boulanger et al., 1994). Femoral venous access may not be possible because these patients usually have severe intertrigo. The use of Doppler ultrasound-guided techniques to obtain central venous access in high-risk patients has been shown to reduce the number of needle passes to cannulate the vein, resulting in a reduction in the incidence of complications (Gratz et al. , 1994). Currently available ultrasound devices can only visualize structures between 1 cm and 4 cm deep and are therefore of limited value in morbidly obese patients. A proactive approach with early placement of a peripherally inserted line (PIC) or tunneled central catheter inserted by an interventional radiologist is recommended. Scrupulous attention is essential in maintaining the sterility of the catheter insertion site (Gratz et al., 1994). Portable bedside radiographs are usually of poor quality in the obese patient, limiting the value of this important diagnostic tool. Abdominal and pelvic ultrasound is limited by the extensive abdominal wall and intra-abdominal fat. Percutaneous aspiration and drainage of intraperitoneal and retroperitoneal collections may be hindered by obese body habitus. Most computed tomography and magnetic resonance imaging tables have weight restrictions (about 300 to 350 pounds) that prohibit imaging morbidly obese patients. Many veterinary hospitals have CT scanners that can accommodate large animals, and some may be willing to scan morbidly obese patients who exceed the weight limits of human scanners. Summary The obesity epidemic is already having major effects on population health. Obesity develops in an individual when energy intake exceeds energy expenditure for a long period. The biological processes that regulate energy balance are very tightly regulated. However, these appetite control mechanisms can easily be overwhelmed by the desire to eat when not hungry if attractive food is provided in inductive contexts. Control pathways include short-term signaling of hunger and satiety with hormones derived from the gastrointestinal tract to the central nervous system, long-term signaling of energy stores via leptin and insulin to the brain, and control of metabolism. Rare genetic syndromes that present in early childhood with severe obesity (such as leptin deficiency and mutations in the pro-opiomelanocortin gene) demonstrate that these pathways are biologically important in humans. Most obesity develops as a result of modern lifestyles in genetically predisposed individuals. These changes include an increase in the consumption of.