Prevention Of Deep Venous Thrombosis In Obese: [Essay Example], 1839 words GradesFixer
exit-popup-close

Haven't found the right essay?

Get an expert to write your essay!

exit-popup-print

Professional writers and researchers

exit-popup-quotes

Sources and citation are provided

exit-popup-clock

3 hour delivery

exit-popup-persone
close
This essay has been submitted by a student. This is not an example of the work written by professional essay writers.

Prevention Of Deep Venous Thrombosis In Obese

Download Print

Pssst… we can write an original essay just for you.

Any subject. Any type of essay.

We’ll even meet a 3-hour deadline.

Get your price

121 writers online

blank-ico
Download PDF

The high risk of thromboembolic disease in obese ICU patients warrants an aggressive approach toward prevention of deep venous 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 the ICU. Deep venous 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 an inferior vena caval filter should be Considered (Meilahn et al., 1996).

Endotracheal intubation can be a daunting experience in 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 the inexperienced practioner, and equipment for urgent airway management (including surgical airway instruments) should be readily avaliable (Williamson et al., 1993).

Management considerations in cardiac pateints admitted to ICU Morbid obesity is characterized by an increase in total blood volume and resting cardiac output. Both increase in direct proportion to the amount the patient weighs over the ideal body weight (IBW). The increment increase in cardiac output is related solely to an increase in stroke volume, with the heart rate being unchanged. The cardiac 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 of systemic vascular resistance in normotensive patients. De Divitiis and coworkers performed left- and right-heart catheterization in 10 morbidly obese (mean BMI of 48.8) but otherwise healthy individuals. These authors noted that the mean oxygen consumption (VO,) was increased (311 mL/min), and that the VO, increased linearly with increasing body weight. The arteriovenous oxygen difference was normal, however, suggesting that the cardiac output increases primarily to serve the metabolic requirements of excessive fat (De Divitiis et al., 1983).

The distribution of cardiac output has been reported to be similar in obese and lean individual. Although the resting cardiac output is increased, obese patients have been demonstrated to have impaired left ventricular contractility and adepressed ejection fraction, both at rest and after exercise. Decreased myocardial p-adrenergic receptors may contribute to this finding (Rexrode KM et al., 1996). Furthermore, 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 the morbidly obese patient, with superimposed left ventricular hypertrophy. It should be emphasized that use of standard-size 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 early filling abnormalities has been reported to be an early indicator of cardiac involvement in obesity (Berkalp B et al., 1995). Electrocardiographic changes with obesity include a leftward shift of the QRS axis and an increase in the PR, QRS, and QTc intervals. In general, the left ventricular filling pressure is elevated in obese patients because of the combination of increased preload and reduced ventricular distensibility (Backman L et al., 1983 ).

In general, the left ventricular filling pressure is elevated in obese patients because of 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 series of patients. Consequently, fluid loading is poorly tolerated by the obese patient (De Divitiis et al., 1983). Drug dosing considerations in critically obese patints. The distribution, metabolism, protein binding, and clearance of many drugs are altered by the physiologic changes associated with obesity (Abemethy & Greenblatt, 1982).

Some of these pharmacokinetic changes may, however, negate the consequences of others and the pharmacokinetic alterations may differ in the morbidly obese as compared with the mildly or moderately obese individual. In addition, the patient’s underlying disease may substantially influence a drug’s pharmacokinetic properties. The net pharmacologic alteration in any patient is, therefore, often uncertain. Nevertheless, for a number of drugs used in the ICU, most notably digoxin, aminophylline, aminoglycosides, and cyclosporine, drug toxicity may occur if the patients are dosed based on their actual body weight. The oral absorption of drugs remains essentially unchanged in the obese patient. The volume of distribution (Vd) of drugs in obese patients is largely dependent on the lipophilicity of the drug (Blouin et al., 1987 ).

The Vd of drugs that are weakly lipophilic (aminoglycosides, quinolones) is moderately increased when compared with the situation in normal individuals, but the Vd corrected by actual body weight is significantly smaller. The Vd is increased for many, but not all, lipophilic drugs. The clearance of most drugs that are hepatically metabolized is not reduced. For drugs that are renally excreted, elimination will depend on the 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 dysfunction, the creatinine clearance, as calculated using standard formulae, correlates very poorly with the measured creatinine clearance.In the obese patient with renal dysfunction, the dosing regimen of renally excreted drugs should be based on the measured creatinine clearance (Blouin et al ., 1987). As a consequence of the complexity of the pharmacokinetic changes that may 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 drugs it is unclear if weight related dosage adjustments should be made and whether these adjustments should be based on the actual body weight, IBW, or a percentage of the actual body weight. Dosing recommendations for drugs that are commonly used in the ICU are listed in the table 3 below (Abemethy & Greenblatt, 1982). Because of the limited and sometimes conflicting data on which these recommendations are based, monitoring of clinical endpoints, signs of toxicity, clinical response, and serum drug levels (when available) are essential (Abemethy & Greenblatt , 1982).

Obtaining adequate venous access in another major problem in the critically ill obese ICU patient. Poor peripheral venous sites in obese patients necessitate more frequent use of central venous access. Ashort stubby neck, loss of physical landmarks, and a greater skin-blood vessel distance make internal jugular and subclavian vein cannulation technically difficult (Boulanger et al., 1994) this difficulty results in a higher incidence of catheter malpositions and local puncture complications. A greater number of skin punctures during catheter insertion and delayed catheter changes may lead to more catheter-related infections and thrombos (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 for obtaining central venous access in high-risk patients has been demonstrated to reduce the number of needle passes to cannulate the vein, with a reduction in the incidence of complications (Gratz et al., 1994) The portable vascular access ultrasound devices currently available can only image structures between 1 cm to 4 cm deep and are therefore of limited value in morbidly obese patients. A proactive approach with the early placement of a peripherally inserted line (PIC) or tunneled central catheter inserted by an interventional radiologist is recommended. Scrupulous attention in maintaining the sterility of the catheter insertion site is essential (Gratz et al., 1994).

Portable bedside radiographs are usually of very poor quality in the obese patient, limiting the value of this important diagnostic tool. 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. Most computed tomography and magnetic resonance imaging tables have weight restrictions (about 300 to 350 lbs) that prohibit imaging of morbidly obese patients. Many animal 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 the human scanners.

Summary

The epidemic of obesity is already having major effects on population health. Obesity develops in an individual when energy intake exceeds energy expenditure over a long period. The biological processes regulating energy balance are very tightly regulated. However, these mechanisms of appetite control can easily be overwhelmed by a willingness to eat when not hungry if attractive food is provided in inductive settings. Control pathways include short-term signalling of hunger and satiety with hormones derived from the gastrointestinal tract to the central nervous system, long-term signalling 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 susceptible individuals.

These changes include increased consumption of high-energy food at the same time as physical activity levels have declined dramatically; in many societies less affluent people seem to be most at risk. Other causes of obesity that should be considered include drugs that increase appetite and structural damage to areas of the central nervous system involved in appetite control, such as the hypothalamus Generally, recent data indicates a positive effect on outcome of obese compared to non obese patients presenting at the ICU irrespective of respiratory management in terms of thirty day and one year survival. When mechanical ventilation is required in obese patients, physiological differences in pulmonary function have to be taken into account.

Generally, large multi- centered studies on respiratory management of obese patients in the ICU are still needed. Concerning patient positioning, there is data supporting that a sitting posture or PP in patients with ARDS may reduce the pressure applied onto the chest by adipose tissue leading to an increase in compliance and FRC (functional residual capacity). Adjusting the body position may aid to avoid the need for high ventilatory pressures and thus, ventilator associated lung injury may be reduced. Another possible maneuver to increase pulmonary compliance and facilitate mechanical ventilation is a reduction or cessation of general anesthesia and early tracheotomy. The association of obesity with sepsis mortality revealed mixed results.

Three studies reported no significant association between obesity and mortality, 1 study observed increased mortality among obese patients with bacteremia whereas 3 studies found decreased mortality among obese patients. Clinicians are facedwith a number of challengeswhilemanaging obese patients with sepsis and should be mindful of the impact of obesity on antibiotics administration, fluid resuscitation, and ventilator management. Also increasing BMI seems to be strongly associated with increased rates of HIT in intensive care unit patients. The management of the morbidly obese critically ill patient is a challenging and formidable task. A better understanding of the pathophysiologic changes that occur with obesity and the complications unique to this group of patients may improve their outcome.

Remember: This is just a sample from a fellow student.

Your time is important. Let us write you an essay from scratch

100% plagiarism free

Sources and citations are provided

Cite this Essay

To export a reference to this article please select a referencing style below:

GradesFixer. (2020). Prevention Of Deep Venous Thrombosis In Obese. Retrived from https://gradesfixer.com/free-essay-examples/prevention-of-deep-venous-thrombosis-in-obese/
GradesFixer. "Prevention Of Deep Venous Thrombosis In Obese." GradesFixer, 16 Mar. 2020, https://gradesfixer.com/free-essay-examples/prevention-of-deep-venous-thrombosis-in-obese/
GradesFixer, 2020. Prevention Of Deep Venous Thrombosis In Obese. [online] Available at: <https://gradesfixer.com/free-essay-examples/prevention-of-deep-venous-thrombosis-in-obese/> [Accessed 12 July 2020].
GradesFixer. Prevention Of Deep Venous Thrombosis In Obese [Internet]. GradesFixer; 2020 [cited 2020 March 16]. Available from: https://gradesfixer.com/free-essay-examples/prevention-of-deep-venous-thrombosis-in-obese/
copy to clipboard
close

Sorry, copying is not allowed on our website. If you’d like this or any other sample, we’ll happily email it to you.

    By clicking “Send”, you agree to our Terms of service and Privacy statement. We will occasionally send you account related emails.

    close

    Attention! this essay is not unique. You can get 100% plagiarism FREE essay in 30sec

    Recieve 100% plagiarism-Free paper just for 4.99$ on email
    get unique paper
    *Public papers are open and may contain not unique content
    download public sample
    close

    Sorry, we cannot unicalize this essay. You can order Unique paper and our professionals Rewrite it for you

    close

    Thanks!

    Your essay sample has been sent.

    Want us to write one just for you? We can custom edit this essay into an original, 100% plagiarism free essay.

    thanks-icon Order now
    boy

    Hi there!

    Are you interested in getting a customized paper?

    Check it out!
    Having trouble finding the perfect essay? We’ve got you covered. Hire a writer

    GradesFixer.com uses cookies. By continuing we’ll assume you board with our cookie policy.