The high risk of thromboembolic disease in obese intensive care patients warrants an aggressive approach to 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 patients in whom anticoagulation is contraindicated, prophylactic placement of an inferior vena cava filter should be considered (Meilahn et al., 1996). Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay Endotracheal intubation can be a daunting experience in the morbidly obese patient and possibly the intensivist's worst nightmare. In the Australian incident surveillance study, obesity with limited neck mobility and limited mouth opening accounted for the majority of cases of difficult intubation. In obese patients, endotracheal intubation should not be attempted by an inexperienced practitioner, and equipment necessary for urgent airway management (including surgical airway instruments) should be readily available (Williamson et al., 1993). Management considerations for cardiac conditions admitted to the ICU. characterized by an increase in total blood volume and cardiac output at rest. Both increase in direct proportion to the patient's weight relative to ideal body weight (IBW). The progressive increase in cardiac output is only linked to an increase in stroke volume, the heart rate remaining unchanged. Cardiac index and stroke 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 people who were morbidly obese (mean BMI 48.8) but otherwise healthy. These authors noted that mean oxygen consumption (VO,) increased (311 ml/min) and that VO increased linearly with increasing body weight. The arteriovenous oxygen difference was normal, however, 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 impaired left ventricular contractility and decreased ejection fraction, both at rest and after exercise. A decrease in 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, leading to left ventricular dilation and hypertrophy. These changes are linked to the degree and duration of obesity (Berkalp B et al., 1995). Systemic hypertension is common in patients suffering from morbid obesity, with superimposed left ventricular hypertrophy. It should be emphasized that the use of standard size sphygmomanometry cuffs will result in inaccurate blood pressure recordings and thatAppropriately sized cuffs should therefore be used. Diastolic dysfunction with a prolonged relaxation phase and early filling abnormalities would be an early indicator of cardiac damage in obesity (Berkalp B et al., 1995). Obesity-related electrocardiographic changes 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 the 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 patient series. Consequently, the fluid load is poorly tolerated by the obese patient (De Divitiis et al., 1983). Medication dosing considerations in severely obese patients. The distribution, metabolism, protein binding, and clearance of many drugs are altered by the physiological changes associated with obesity (Abemethy & Greenblatt, 1982). However, some of these pharmacokinetic changes may override the consequences of others and the pharmacokinetic alterations may differ. in morbidly obese individuals compared to mildly or moderately obese individuals. Additionally, the patient's underlying disease can significantly influence the pharmacokinetic properties of a drug. The net pharmacological alteration in any patient is therefore often uncertain. However, for a number of drugs used in intensive care, including digoxin, aminophylline, aminoglycosides, and cyclosporine, drug toxicity can occur if patients receive a dose based on their actual body weight. Oral absorption of drugs remains essentially unchanged in the obese patient. The volume of distribution (Vd) of drugs in obese patients depends largely on the lipophilic nature of the drug (Blouin et al., 1987). The Vd of poorly lipophilic drugs (aminoglycosides, quinolones) is moderately increased compared to the volume of distribution (Vd) of drugs in obese patients. 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 drugs metabolized in the liver is not reduced. For drugs excreted by the kidneys, 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 by glomerular filtration (Blouin et al., 1982). In obese patients with renal impairment, creatinine clearance, as calculated using standard formulas, correlates very poorly with measured creatinine clearance. In obese patients with renal dysfunction, the dosage regimen of renally excreted drugs should be based on measured creatinine clearance (Blouin et al., 1987). Due to the complexity of pharmacokinetic changes that can occur in obese patients and the limited data available on many medications, there are inconsistencies and disagreements in the literature regarding drug dosing in obesity (Blouin et al., 1987). For many drugs it is unclear whether weight-based dosage adjustments should be made.made and whether these adjustments should be based on actual body weight, IBW or a percentage of actual body weight. Dosage recommendations for drugs commonly used in intensive care are listed in Table 3 below (Abemethy & Greenblatt, 1982). Due to the limited and sometimes conflicting data on which these recommendations are based, monitoring of clinical parameters, signs of toxicity, clinical response, and serum drug levels (when available) is essential (Abemethy & Greenblatt, 1982 ). another major problem in the critically ill obese patient in intensive care. Poor peripheral venous sites in obese patients require more frequent use of central venous access. A short and stocky neck, a loss of physical landmarks and a greater distance between the skin and the blood vessels make cannulation of the internal jugular and subclavian veins technically difficult (Boulanger et al., 1994), this difficulty results in a higher incidence of catheter malpositions and local puncture complications. Greater numbers of skin perforations during catheter insertion and late catheter changes may lead to more catheter-related infections and thromboses (Boulanger et al., 1994). Femoral venous access may not be possible as 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, with a reduction in the incidence of complications (Gratz et al., 1994). Portable vascular access ultrasound devices currently available can only image structures between 1 cm and 4 cm in depth and therefore have limited value in patients with morbid obesity. 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 to maintaining sterility of the catheter insertion site is essential (Gratz et al., 1994). Portable bedside radiographs are generally of very poor quality in the obese patient, limiting the value of this important diagnostic tool. Abdominal and pelvic ultrasound is limited by an extended abdominal wall and intra-abdominal fat. Percutaneous aspiration and drainage of intraperitoneal and retroperitoneal collections may be hampered by obese body habitus. Most CT and magnetic resonance imaging tables have weight restrictions (approximately 300 to 350 pounds) that prohibit imaging of morbidly obese patients. Many veterinary clinics 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 the population health. Obesity develops in an individual when energy intake exceeds energy expenditure over a long period of time. Biological processes regulating energy balance are very tightly regulated. However, these appetite control mechanisms can easily be overridden by the drive to eat without feeling hungry if attractive food is provided in an inductive setting. 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.