Erin McLean



Morbid Obesity Case StudyErin McLeanBaptist Health System Dietetic InternshipThe obesity epidemic is a growing health concern in the United States as well as in the world. According to data from the most recent National Health and Nutrition Examination Survey, 35.7% of adults in the United States are obese based on measured height and weight (Ogden, Carroll, Kit, & Flegal, 2012). More specifically, a recent study (Sturm & Hattori, 2013) found that approximately 6.6% of adult Americans in 2010 had a morbidly obese BMI status. This case study examines a patient diagnosed with morbid obesity who presented to the hospital for debridement of a groin abscess. It examines the patient’s health and medical history and provides an in-depth review of morbid obesity, including its nutritional impact on the patient. In addition, the nutrition care process is reviewed.Patient ProfileThe patient is a 51 year old Hispanic male who was admitted on January 25, 2014 and discharged to hospice twenty-four days later on February 17, 2014. The patient was admitted to the hospital for a lump that presented on his right groin. The lump grew in size and began draining pustular fluid approximately three weeks prior to hospital admission. The patient reported that the pain in his lower abdominal region became progressively worse with a ten out of ten pain rating upon admission. The patient also reported that the pain was accompanied by some nausea and vomiting.The patient was separated from his wife and had no reported children. Due to his morbid obesity, the patient was cared for at home by his brother and sister. He had no prior history of alcohol or illicit drug abuse. Information regarding whether the patient was employed was not disclosed in the medical record nor was his religious affiliation or education level.The patient had a past medical history of morbid obesity, hypertension, chronic lymphedema, sleep apnea, anxiety, and a remote history of seizure disorder. He had a past surgical history of cholecystectomy and gunshot wound repairment (the location of the gunshot wound was not specified). He had a family history of diabetes mellitus (DM). Medications that the patient took at home were not listed in the electronic medical record. The patient was 5’7” and upon admission weighed 250 kg. Before admission, the patient consumed solids and liquids with ease and exhibited no dental or swallowing difficulties. Likewise, he had no reported issues with elimination. The patient did, however, present with some digestive issues before admission, namely nausea and vomiting. According to the wife, the patient had lost weight prior to admission by eating small, frequent meals throughout the day. She stated, however, that she was unaware of the exact amount of weight lost by the patient and the duration over which the loss occurred. The dietitian who initially assessed the patient reported that he had lost 91 kg prior to admission by eating mostly fruits and vegetables. Due to the patient’s morbid obesity, he was mostly bedbound before admission. The patient did, however, have gross movement of his extremities. In addition, the patient had a prior diagnosis of sleep apnea which was related to his morbid obesity. The patient, however, had not been using a continuous positive airway pressure machine to treat the condition. Disease BackgroundDefinitionThe patient was initially diagnosed with a right groin abscess, cellulitis, and morbid obesity upon admission but developed several other conditions throughout his hospitalization. An abscess is a collection of pus composed primarily of necrotic tissue, bacteria, white blood cells, and fluid which can cause painful swelling and inflammation (Dugdale, 2012). Abscesses can form almost anywhere in the body and are caused by the immune system attacking infected tissue. Cellulitis is a potentially serious skin infection caused by bacteria which can affect the skin’s surface as well as underlying tissue beneath the skin (“Cellulitis,” 2012). According to the physician, both the abscess and the cellulitis were caused by Streptococcus agalactiae and methicillin-sensitive?Staphylococcus aureus. This was determined after a fluid sample drawn from the patient’s abscess tested positive for these organisms. The patient presented to the hospital with a body mass index (BMI) of 91 kg/m2, placing him in the class III, morbidly obese category for BMI. The following table depicts BMI weight classifications (Hurt & Frazier, 2012): BMI ClassificationWeight StatusBMI (kg/m2)UnderweightBMI ≤ 18.49Normal weightBMI ≥ 18.5 to 24.9OverweightBMI ≥ 25 to 29.9Obesity class IBMI ≥ 30 to 34.9Obesity class IIBMI ≥ 35-39.9Obesity class IIIBMI ≥ 40 Figure 1. BMI classification. In general, obesity is a condition marked by the excessive accumulation of fat in the body (“Obesity,” n.d.). It is associated with many different comorbid conditions, including type II DM, coronary artery disease (CAD), and sleep apnea as well as various cancers. Upon admission, the patient had no previous diagnosis of DM. However, after a hemoglobin A1c (HbA1c) test was conducted, he was found to have a HbA1c of 13.6%, indicating uncontrolled type II DM. Type II DM is caused by a combination of insulin resistance and, to a lesser extent, a lack of insulin production by the pancreas. It is characterized by elevated blood sugar levels due to cellular resistance to insulin, the hormone needed to transport glucose into cells. This condition is more common in overweight and obese individuals since increased fat stores often impair insulin function (Wisse, 2013). The patient underwent surgery for debridement of his right groin abscess on the same dayhe was admitted to the hospital. While he tolerated the procedure well, he was unable to be extubated after surgery since he had developed acute respiratory failure (ARF). According to the physician, this condition was secondary to obesity hypoventilation syndrome. In general, ARF is characterized by decreased blood oxygenation and elevated arterial carbon dioxide levels, termed hypoxemia and hypercapnia respectively (Kaynar & Sharma, 2012). Obesity hypoventilation syndrome is caused by both a defect in the region of the brain that controls breathing and by excessive weight that presses against the chest wall (Dugdale, 2012). The inability of the patient to be weaned from the ventilator near the end of his stay was attributed to the combination of septic shock and pneumonia which he later developed as well as his morbid obesity. The patient also developed sepsis early into his admission which later developed into septic shock near the end of his hospitalization. According to the physician, the cause of the sepsis could likely be attributed to bacteria from the right groin abscess as well as a fungal urinary tract infection (UTI). In general, sepsis occurs when the body mounts a strong immune response to fight an infection. However, this systemic inflammatory response can cause organ damage, leading to conditions such as acute respiratory distress syndrome and acute kidney injury (AKI) (Venes, 2009). In severe sepsis, or septic shock, a life-threatening condition known as hypotension, or low blood pressure, occurs. The physician ascribed the development of septic shock to the combination of aspiration pneumonia, an infection in the lungs that can be caused by the inhalation of food, gastric secretions, or other substances, and the fungal UTI. Near the end of the patient’s hospital stay, he developed AKI. This condition is defined as the inability of the kidneys to filter waste products from the blood and to maintain adequate fluid and electrolyte levels in the body. The onset of AKI occurs rapidly over a few hours to a few days (Dugdale & Lin, 2012). In some cases, AKI is reversible and normal kidney function can be restored. However, AKI can also lead to irreversible kidney damage, requiring dialysis or a kidney transplant for management.The patient was also diagnosed with a possible ischemic bowel. This condition is the result of inadequate blood supply to the bowel and occurs when an artery supplying the bowel with blood becomes narrowed or obstructed (Bearden, 2013). An official diagnosis of ischemic bowel disease could not be made since x-ray exams of his abdomen were severely limited due to the patient’s obese body habitus. Similarly, a computed tomography scan could not be utilized to evaluate the patient due to his morbid obesity.Pathophysiology According to the laws of thermodynamics, energy intake that exceeds energy expenditure over a period of time can result in the pathogenesis of obesity (Hurt & Frazier, 2012). However, other factors account for obesity including the intricate interplay between the central nervous system and hormones involved in appetite regulation and weight management. Leptin is a hormone that is produced and secreted by white adipose tissue. It moderates long-term energy balance by acting on the hypothalamus to stimulate reduced food intake and increased energy expenditure. The level of leptin that circulates in the body is directly proportional to the amount of total fat mass in the body (Beckman, Beckman, & Earthman, 2010). Therefore, individuals with increased body fat likewise have increased levels of circulating leptin. Similarly, those with decreased body fat have decreased levels of circulating leptin. Elevated leptin levels do not, however, prevent the progression of obesity despite its role in energy balance. Instead, recent research suggests that leptin resistance is one of many possible culprits involved in the development of obesity rather than leptin deficiency (Beckman, Beckman, & Earthman, 2010).Insulin is another adiposity signal that indicates the amount of total fat mass in the body. In general, insulin is synthesized by pancreatic beta cells and is involved in many functions including food intake regulation and the production and storage of fat. As with leptin, the amount of fasting insulin levels is directly proportional to the amount of fat mass in the body (Mahan, Escott-Stump, & Raymond, 2012). In obese individuals, elevated adiposity can cause reduced insulin sensitivity as well as insulin resistance. Individuals with impaired insulin action also have a decreased level of thermogenesis, further contributing to adiposity (Mahan, Escott-Stump, & Raymond, 2012). Some research suggests that insulin resistance may even be a contributing factor in the development of obesity rather than just a symptom of it (Perry & Wang, 2012).While leptin and insulin indicate long-term energy status, hormones secreted by the gut including ghrelin, glucagon-like peptide (GLP-1), and peptide YY (PYY) are believed to play an integral role in appetite (Perry & Wang, 2012). Ghrelin is produced primarily in the stomach and stimulates the appetite by acting on the hypothalamus, causing sensations of hunger. Compared to normal-weight individuals, fasting ghrelin levels in obese individuals are lower (Perry & Wang, 2012). Nevertheless, ghrelin has been suspected to play a role in the pathophysiology of obesity due to the negligible and sometimes absent decrease in circulating ghrelin levels post-prandially in obese individuals, an event not observed in normal-weight individuals. GLP-1 is a gut hormone released in the ileum and colon in response to food ingestion. The hormone regulates the appetite by decreasing sensations of hunger and imparting satiety. GLP-1 regulates the appetite in this manner in both lean and obese individuals, making the peripheral administration of this hormone a current topic of research for weight loss therapy (Beckman, Beckman, & Earthman, 2010). Similarly, it is proposed that circulating levels of this hormone are elevated in lean individuals and decreased in obese individuals, but more research is needed to confirm these findings (Beckman, Beckman, & Earthman, 2010).Another gut hormone is PPY which, like GLP-1, is released in the ileum and colon with the ingestion of food. PPY is involved in appetite management by inducing satiety when secreted. Some research has found that PPY levels in both the fasting and postprandial state are reduced in obese individuals and higher in lean individuals (Beckman, Beckman, & Earthman, 2010).Symptoms/Clinical ManifestationsThe increased accumulation of adipose tissue primarily in the subcutaneous tissue and in the abdominal region leads to the pathogenesis of obesity and morbid obesity (Brethauer, Kashyap, & Schauer, 2013). Adipocytes increase in number and size as obesity develops and the effects of this phenomenon can have a detrimental systemic impact on the body.More than thirty comorbidities have been linked to morbid obesity including insulin resistance and DM which presents in approximately 15 to 25% of obese individuals (Brethauer, Kashyap, & Schauer, 2013). The development of CAD, the hypercoagulable state, and other vascular diseases is attributable to inflammation associated with morbid obesity. Pulmonary issues that often present in conjunction with morbid obesity include obstructive sleep apnea, asthma, and obesity hypoventilation syndrome. Gastroesophageal reflux, abdominal hernias, chronic venous insufficiency, and urinary incontinence can also occur due to the pressure exerted by the abdominal fat on the body. Dyslipidemia, hypertension, nonalcoholic fatty liver disease, cancer, sex hormone disorders, urinary tract infections, skin infections, headaches, and depression are other comorbid conditions associated with severe obesity (Brethauer, Kashyap, & Schauer, 2013). EtiologyNumerous factors contribute to the etiology of morbid obesity including diet, physical activity level, sleep deprivation, heredity, obesogens, and pathogens. Diets characterized by frequent meals high in unhealthy fats, red meats, refined grains, and sugar-laden beverages are a major contributing factor to the development of morbid obesity (“Obesity causes,” n.d.). Similarly, the growing obesogenic environment makes access to energy-dense foods easier and cheaper (Hurt & Frazier, 2012). Disordered eating habits such as skipping meals, compulsive overeating, and binge eating can also cause morbid obesity as well as the frequent consumption of fast food.Leading an overall sedentary lifestyle with minimal physical activity is another major factor involved in the development of morbid obesity. A lack of physical activity coupled with chronic overeating is a major cause of weight gain. Exercise is being replaced by activities such as watching television and movies, playing video games, and surfing the Internet which require minimal energy expenditure (Mahan, Escott-Stump, & Raymond, 2012).Chronic sleep deprivation can likewise play a role in the etiology of morbid obesity since it alters endocrine regulation. In particular, the lack of adequate sleep can increase the effect of hormones responsible for appetite, leading to excessive caloric intake (Mahan, Escott-Stump, & Raymond, 2012). More specifically, it can change the composition, quantity, and timing of food intake throughout the day, further exacerbating weight gain. Heredity also plays a role in the development of morbid obesity. Genes, however, are not the primary or sole cause of obesity as many believe but rather a contributing factor to weightgain just as physical inactivity or an unhealthy diet is (“Obesity causes,” n.d.). In general, many factors are influenced by genes including appetite and satiety, resting metabolic rate, the quantity and size of adipose cells, and the distribution of fat mass in the body (Mahan, Escott-Stump, & Raymond, 2012). Defects in the genes controlling these factors can cause excessive weight gain and eventually lead to morbid obesity. Similarly, genes involved in the development of obesity can be activated or deactivated by nutritional and lifestyle factors. Chemical compounds known as obesogens alter lipid metabolism and promote fat accumulation in the body, predisposing some individuals to obesity. These chemical agents can be pharmaceutical, industrial, or dietary compounds which act as endocrine disruptors (Holtcamp, 2012). In general, these agents disrupt lipid metabolism, promote fat storage in the body, alter hormonal signals pertaining to appetite and satiety, modify energy balance, and shift metabolic set points (Mahan, Escott-Stump, & Raymond, 2012). Examples of pharmaceutical obesogens include thiazolidinediones which are used in the treatment of type II DM, selective serotonin reuptake inhibitors which are used to treat depression, and diethylstilbestrol which was used to prevent pregnancy complications (the drug is no longer manufactured in the United States). Industrial obesogens include tributyltin and triphenyltin compounds, ingredients used in some biocides, bisphenol A, a compound used to synthesize plastics and epoxy resins, perfluorooctanoic acid, a substance used in the production of Teflon? and other fluorotelomers, and diethylhexyl phthalate, a compound utilized to increase flexibility and plasticity in products. Dietary obesogens include monosodium glutamate, a flavor enhancer used in food, and genistein, a phytoestrogen found naturally in soybeans and other food sources (Holtcamp, 2012).Pathogens have also been suspected in the development of obesity, but more research is needed to confirm whether they contribute significantly to the condition. Currently, at least ten infectious agents have been identified and implicated in adipogenesis, including bacteria, viruses, gut microflora, and prions (Mahan, Escott-Stump, & Raymond, 2012). TreatmentLifestyle modification. Lifestyle modification is essential to the management of morbid obesity and encompasses behavior modification, diet intervention, and physical activity. According to Mahan, Escott-Stump, and Raymond (2012), behavior modification focuses on modifying an individual’s “environment, nutritional intake, and physical activity by using goal setting, stimulus control, problem solving, cognitive restructuring, self-monitoring, and relapse prevention.” (p. 473). These strategies assist people in defining clear-cut goals concerning their weight, becoming aware of environmental stimuli that can undermine healthy behavior modifications, and identifying and correcting negative thought patterns and resultant emotions that sabotage their weight loss efforts.Many different diet interventions exist to promote weight reduction. A calorie restriction diet is the most common method utilized for weight loss. This diet consists of a balanced macronutrient composition and contains adequate amounts of necessary nutrients but employs an overall energy deficit to promote weight loss. In general, a 500 to 1000 kcal/d deficit causes the body to utilize fat stores to promote weight loss of one to two pounds per week (Mahan, Escott-Stump, & Raymond, 2012). Meal replacement diets are another common and effective method for weight reduction. Meal replacement beverages, nutrition bars, and packaged meals can be used to replace one to two meals per day (three meals a day if it is a calorie-controlled packaged meal). These products assist individuals who struggle with self-selection of food and who have difficulty with controlling for portion size (Seagle, Strain, Makris, & Reeves, 2009). Many people also utilize commercial diet programs that use a variety of weight loss methods including calorie restriction, meal replacement products, education, and exercise. The evidence to support the effectiveness of these programs is minimal with the exception of Weight Watchers (Mahan, Escott-Stump, & Raymond, 2012).Physical activity is another important component of lifestyle modification. It facilitates energy expenditure, improves comorbidities linked to obesity, and promotes an overall sense of wellbeing. However, physical activity will not result in impactful weight loss without an accompanying decrease in caloric intake. According to the 2008 Physical Activity Guidelines for Americans, adults should engage in a minimum of 150 minutes of moderate-intensity aerobic exercise per week or 75 minutes of vigorous-intensity aerobic exercise per week (“Physical Activity Guidelines,” 2008). In addition, adults should engage in moderate-intensity strength training exercise at least twice a week. Pharmaceutical management. Only a handful of medications are currently approved by the Food and Drug Administration (FDA) for the treatment of obesity. In order to be eligible for obesity pharmacotherapy, individuals must have a BMI of 30 kg/m2 or greater or have a BMI of 27 to 29 kg/m2 with at least one obesity-related comorbidity (“Prescription medications,” 2013). Pharmaceutical management of obesity, however, should be used in conjunction with lifestyle modifications to augment weight loss results. Orlistat, lorcaserin, and phentermine-topiramate are three long-term obesity treatment drugs currently approved by the FDA. Orlistat, known as Xenical? when sold as a prescription drug or Alli? when sold over-the-counter, reduces fat absorption in the body. Lorcaserin is marketed under its trade name Belviq? and decreases appetite by acting on serotonin receptors in the brain. Phentermine-topiramate, sold as the prescription drug Qsymia?, is a combination of two drugs: phentermine which decreases appetite and topiramate which treats seizures as well as migraine headaches (“Prescription medications,” 2013). There are several prescription drugs approved for short-term use (twelve weeks maximum) by the FDA which induce satiety by increasing chemicals in the brain that influence appetite.Surgical intervention. There are several different types of bariatric surgeries available to treat obesity. These surgical procedures are classified as restrictive, malabsorptive, or a combination of both restrictive and malabsorptive. In general, restrictive procedures involve significantly decreasing the stomach’s capacity to hold food, thereby limiting the amount of calories a person can ingest. In the United States, the laparoscopic adjustable gastric banding (LAGB) is the most popular restrictive procedure and involves placing an inflatable silicone band around the upper portion of the stomach (Kulick, Hark, & Deen, 2010). The resultant gastric pouch that is created limits the amount of food that can be ingested at one time. An infusion port connected to the band by a small tube is placed on the upper abdominal wall below the skin. Adjustments to the band size are made by inserting a syringe into the infusion port and either injecting or withdrawing saline solution (“Gastric banding,” 2012). The sleeve gastrectomy (SG) is another type of restrictive procedure which removes approximately 75% of the stomach, leaving a small gastric sleeve intact (“Sleeve gastrectomy,” n.d.). Due to the reduced size of the stomach, only small quantities of food can be consumed at one time, contributing to weight loss. Also, due to the removal of a large portion of the stomach, the production of appetite regulating hormones is reduced, causing a decrease in appetite.Malabsorptive procedures entail removing considerable portions of the small intestines to impair nutrient absorption, thereby leading to weight loss. Biliopancreatic diversion, duodenal switch, and jejunoileal bypass are all malabsorptive procedures that produce significant weight loss results, but due to metabolic complications that ensue afterwards (protein and calorie malnutrition and micronutrient deficiencies), they are rarely performed (Kulick, Hark, & Deen,2010). The Roux-en-Y gastric bypass (RYGB) is primarily considered a restrictive procedure but contains malabsorptive elements as well. In the United States, RYGB is considered the gold standard procedure for surgical weight loss due to the significant amount of weight that can be lost. RYGB involves creating a small gastric pouch by surgically separating it from the rest of the stomach. The gastric pouch is then connected to the mid-jejunum, bypassing the lower stomach, the duodenum, and the first section of the jejunum (“Roux-en-Y,” n.d.). The small gastric pouch restricts food intake while the reconfigured small bowel has less opportunity for nutrient absorption due to its reduced size, thus promoting weight loss. Likewise, hormonal and neural changes resulting from the procedure may also contribute to weight loss (Kulick, Hark, & Deen, 2010). A study by Carlin et al. (2013) was conducted to analyze the comparative effectiveness of three differing bariatric procedures, namely, SG, RYGB, and LAGB. Due to the lack of published studies concerning the effectiveness of SG for the treatment of severe obesity, insurance carriers and other payers have largely declined routine coverage for this procedure. A total of 2,949 patients who underwent SG were matched based on twenty-three characteristics to the same number of patients who underwent RYGB and LAGB. Data on the patients and the procedures they underwent was obtained from a statewide clinical registry that had been externally audited. Several outcomes were examined including weight loss, complications that arose within 30 days of the procedure, remission of obesity-related comorbidities at 1, 2, and 3 years after the procedure, and quality of life. Results showed that weight loss at 1 year for SG was 13% lower compared to RYGB (p < 0.0001) and 77% higher compared to LAGB (p < 0.0001). Weight loss in patients plateaued or rebounded in all three procedure groups at years 2 and 3. Overall complication rates in patients who underwent SG were lower compared to RYGB (p < 0.0001) and higher compared to those who underwent LAGB (p < 0.0001). In addition, severe complications rates for SG were similar to RYGB (p = 0.736) but higher compared to LAGB (p < 0.0001). Remission rates for comorbidities in patients who underwent SG were similar to those who underwent RYGB but differed compared to LAGB patients (no measure of statistical significance was provided). The researchers concluded that due to the greater weight loss observed after SG compared to LAGB as well as the decreased complication rates compared to RYGB, insurance carriers should provide routine coverage for this bariatric procedure. Treatment specific to patient. Treatment centered primarily on stabilizing the patient’s overall condition, which consisted of multiple diagnoses, rather than the exclusive treatment of his morbid obesity. Upon admission, the patient underwent surgical debridement of his right groin abscess with subsequent placement of two large wound vacuums to assist in wound healing. While the patient tolerated the procedure well, he remained intubated after the surgery and later underwent a tracheostomy since he was unable to weaned from the ventilator. Shortly after his abscess debridement surgery, the patient developed a urethral stricture which required the urologist to perform a cystoscopy with the placement of a Foley catheter. Thirteen days into his admission, a percutaneous endoscopic gastrostomy (PEG) tube was placed for the administration of enteral feeds since the patient was unable to eat by mouth. The last procedure the patient underwent was the placement of a dialysis catheter in the right internal jugular vein for dialysis access. The patient received two renal replacement therapy treatments before he was placed in hospice due to the overall deterioration of his conditionNutrition therapy was utilized primarily to decrease the patient’s body weight. The tube feedings the patient received provided only 50% of his estimated daily caloric needs as calculated by the dietitian. Total parenteral nutrition was later provided to the patient due to the suspected ischemic bowel disease, but no information regarding the nutrient composition or rate of this feeding was available in the patient’s electronic medical record after his discharge. The patient was also placed on a variety of medications during his hospital stay including anesthetic, vasocontrictive, analgesic, antianxiety, antidiabetic, antihypertensive, antigerd, diuretic, laxative, anticoagulant, and antimicrobial drugs. Some of these medications included propofol, norepinephrine, fentanyl, lorazepam, insulin lispro, nebivolol, pantoprazole, furosemide, bisacodyl, heparin, and vancomycin. A few of the patient’s medications had the potential to cause drug-nutrient interactions. For example, natural licorice should be avoided when taking nebivolol, an antihypertensive drug, and furosemide, a diuretic, since compounds in this food antagonize the action of these drugs. Pantoprazole, used to decrease gastric acid secretion, can interfere with the absorption of vitamin B12 and iron (Pronsky & Crowe, 2010). Also, bisacodyl, a laxative, should not be taken within 1 hour of consuming milk products or with calcium or magnesium supplements. Doing so can result in nausea and stomach discomfort since these products destroy the coating on bisacodyl tablets. Nutrition InterventionNutrition interventions for morbid obesity differ depending on the condition of the patient. In general, decreasing caloric intake creates a negative energy balance, thereby causing a person to lose weight regardless of the macronutrient composition of the diet. Furthermore, Hurt and Frazier (2012) state that “differences in lost weight and body composition between diets are generally small compared to the overall effect of reducing intake” (p. 608).For ambulatory, morbidly obese patients, nutrition interventions should focus on achieving a 10% decrease in initial body weight over a six month period (Hurt & Frazier, 2012). Weight loss greater than this amount is difficult to sustain, so once the initial goal is reached, efforts should be geared toward maintaining the lost weight. Afterwards, motivated patients can proceed to lose more weight.For critically ill, morbidly obese patients, determining resting metabolic rate (RMR) is critical to reducing poor outcomes related to under- and overfeeding. While indirect calorimetry is considered the gold standard for measuring RMR, multiple factors including availability, cost, and feasibility limit its widespread use in the hospital setting. Instead, predictive equations are utilized to determine the energy needs of patients. In general, the Penn State Equation [PSU(2003b)] should be utilized to determine energy requirements in critically ill, mechanically ventilated, obese adults less than or equal to sixty years of age. Conversely, the Modified Penn State Equation [PSU(2010)] should be used to estimate energy needs in critically ill, mechanically ventilated, obese adults greater than sixty years of age. The equations are as follows (“Critical illness,” 2013):PSU(2003b): RMR (kcal/d) = Mifflin (0.96) + VE?(31) + Tmax?(167) – 6212PSU(2010): RMR (kcal/d) = Mifflin (0.71) + VE?(64) + Tmax(85) – 3085The variable VE is the minute ventilation (L/min) while Tmax is the highest or maximum body temperature in the past 24 hours (centigrade). Mifflin is the Mifflin-St. Jeor equation (Wooley & Frankenfield, 2012). The calorie per kilogram (kcal/kg) method is also used to calculate the energy requirements of critically ill, mechanically ventilated, obese patients. More specifically, the method is often used to determine high protein, hypocaloric feedings in this population group. According to guidelines put forth by the American Society for Parenteral and Enteral Nutrition, 22 to 25 kcal/kg ideal body weight (IBW) per day should be utilized to determine target energy needs in critically ill, obese adults (Hurt & Frazier, 2012). This calorie range provides 60 to 70% of estimated energy requirements for these critically ill, obese individuals. For obesity class III patients, 2.5 g/kg IBW is the recommended protein requirement per day (Hurt & Frazier, 2012). The high protein, hypocaloric feedings are believed to assist in lean body mass and nitrogen balance maintenance while promoting the utilization of fat tissue for energy. However, some research has indicated that the kcal/kg method, when used to determine energy needs in critically ill, mechanically ventilated patients, is incorrect 54% of the time and likewise produces significant errors 43% of the time (Wooley & Frankenfield, 2012).A recent study (Frankenfield, Ashcraft, & Galvan, 2013) was conducted which examined the use of predictive equations to determine energy expenditure in critically ill, morbidly obese and underweight patients. The study’s purpose was to provide validation data on the accuracy of these predictive equations since little data currently exists. The RMR of critically ill, mechanically ventilated patients with a BMI of ≤ 21.0 or ≥ 45.0 kg/m2 was assessed using indirect calorimetry (IC). Various predictive equations were subsequently compared to the IC measurements including the Penn State equation, Ireton-Jones equation, Faisy equation, Harris-Benedict equation, Mifflin-St Jeor equation, and the American College of Chest Physicians (ACCP) standard which utilizes actual weight, metabolically active weight, or IBW. Accuracy was determined when energy expenditure estimations from equations fell within 10% of the IC measurement. Results showed that the Penn State equation had the highest accuracy rate (76%) in morbidly obese patients while the ACCP standard had the lowest accuracy rate when actual body weight was utilized (0%). Similarly, the Penn State equation had the highest accuracy rate (63%) in underweight patients, but when the BMI dropped below 20.5, the accuracy rate fell to 58%. The researchers concluded that for critically ill, morbidly obese patients, the Penn State equation is valid for estimating RMR. For critically ill, underweight patients, the researchers suggested that a modification to the Penn State equation is necessary to improve the accuracy rate. Prognosis While obesity/morbid obesity is not a leading cause of death in the United States or in the world according to surveys conducted by the Centers for Disease Control and the World Health Organization, it does increase an individual’s risk for related comorbidities. Some of these comorbidities include CAD, the leading cause of death in the United States and the world, and stroke, the fourth most common cause of death in the United States the second most common cause in the world (“Leading causes,” 2013; “Top 10,” 2013). Similarly, DM is another obesity-related comorbidity and is the seventh most common cause of death in the United States and the eighth most common cause in the world (“Leading causes,” 2013; “Top 10,” 2013). Cancer is likewise a leading cause of death in the United States and the world. While the risk of developing these comorbidities decrease with weight loss, maintaining the lost weight is often difficult. In general, all obesity-related interventions pose the risk for weight regain. Compared to lifestyle modifications and pharmaceutical management, surgical interventions provide the greatest weight loss results which are often sustained over a longer period of time. Despite this, 20 to 30% of people who undergo bariatric surgery do not achieve successful weight loss results due to weight regain (Stoklossa & Atwal, 2013). In a study by Martino et al. (2011), the relationship between intensive care unit (ICU) outcomes and morbid obesity was examined. Research on critically ill, obese adults has found that outcomes in this patient group are not worse than in normal-weight adults. Research examining outcomes in those with morbid obesity with a BMI ≥ 40 kg/m2 has not been conducted, however. Data was gathered and evaluated from a multicenter international observational study which examined nutrition practices in the ICU. The observational study took place in 355 ICU units in 33 different countries and included data from 2007 to 2009. Patients that were included in the study by Martino et al. were mechanically ventilated adults (≥ 18 years of age) who received treatment in the ICU for more than 72 hours. Comparison of 60-day mortality rate, duration of mechanical ventilation (DMV), length of stay (LOS) in the ICU, and hospital LOS was conducted between morbidly obese and normal-weight patients. Potential cofounders were adjusted for using logistic generalized estimating equations and Cox proportional hazard methods with ICU clustering. A total of 8,813 patients were included in the study of which 3,490 had a normal weight while 348 had a BMI of 40 to 49.9 kg/m2, 118 had a BMI of 50 to 59.9 kg/m2, and 58 had a BMI of 60 kg/m2 or greater. Results showed that critically ill, morbidly obese patients had an improved 60-day mortality rate when compared to normal-weight individuals (p = 0.04), but this was considered nonsignificant after cofounders were adjusted for. Also, morbidly obese patients had a longer DMV (p = 0.0013), ICU LOS (p = 0.0016), and a trend toward a decreased hospital LOS (p = 0.17) compared to normal-weight individuals after adjustment of cofounders. The researchers concluded that morbid obesity is not associated with a decreased survival rate compared to normal-weight patients during critical illness. However, it is associated with increased DMV and ICU LOS.Nutrition Care ProcessNutrition AssessmentDuring the patient’s twenty-four day stay in the hospital, his weight fluctuated from a low of 206.9 kg to a high of 280.1 kg. However, these extreme fluctuations in weight over a short duration were due to error in measurement as well as fluid accumulation in the patient near the end of his hospital stay. In general, the patient’s weight ranged primarily between 260 to 270 kg, with no dry weights recorded. The patient was 5’7” and his BMI was calculated at 91 kg/m2 (264.5 kg was the weight used to calculate BMI), placing him in the obesity class III or morbidly obese category. His IBW was calculated to be 67.3 kg ± 10% while his percent IBW was calculated at 393%. The dietitian who conducted the initial assessment charted that the patient’s usual body weight was 318 kg, placing him at 83% of his usual body weight at the time of admission. The percent weight loss experienced by the patient was considered borderline severe since it occurred in a relatively short timeframe. Many different biochemical labs were drawn to assess the patient’s overall health, to determine organ function, and to determine the presence of infection. The following tables contain the patient’s most pertinent lab values drawn throughout his hospital stay:Basic Metabolic Panel Date01/2602/0202/0802/12Glucose(mg/dL)372, High205, High280, High124, HighBUN(mg/dL)Normal44, High28, High59, HighCreatinine (mg/dL)NormalNormalNormal3.43, HighSodium(mEq/L)131, LowNormalNormalNormalPotassium(mEq/L)NormalNormalNormal6.1, HighChloride(mEq/L)95, LowNormalNormalNormalCO2(mEq/L)23, Low32, High34, HighNormalCalcium (mg/dL)NormalNormalNormalNormalGFR (mL/min/1.73 m2)NormalNormalNormal19, LowFigure 2. Patient’s basic metabolic panel.Renal ProfileDate01/3002/1202/1402/17Glucose (mg/dL)191, High174, High137, High215, HighBUN(mg/dL)Normal62, High32, High74, HighCreatinine (mg/dL)Normal3.81, High2.36, High3.52, HighSodium (mEq/L)133, LowNormalNormalNormalPotassium (mEq/L)Normal5.9, HighNormal5.1, HighChloride (mEq/L) 98, LowNormalNormalNormalCO2(mEq/L)NormalNormalNormalNormalCalcium (mg/dL)NormalNormal7.9, LowNormalAlbumin (gm/dL)1.7, Low1.8, Low1.8, Low1.7, LowPhosphorus (mg/dL) 4.5, HighNormalNormal4.4, HighGFR (mL/min/1.73 m2)Normal17, Low29, Low18, LowFigure 3. Patient’s renal profile. Complete Blood Count Date01/2502/0102/0802/1502/17White Blood Cell (K/uL)23.71, High17.47, HighNormal13.22, High17.29, HighRed Blood Cell (m/ul)4.22, Low3.99, Low2.56, Low2.57, Low2.66, LowHemoglobin (gm/dL)13.0, Low12.6, Low7.9, Low8.0, Low8.4, LowHematocrit (%)NormalNormal27.5, Low26.5, Low28.2, LowFigure 4. Patient’s complete blood count.Other LabsDate01/2602/13Triglycerides (mg/dL)228, HighNo lab drawnLactate(mmol/L )No lab drawn5.5, HighFigure 5. Patient’s other labs.The patient’s glucose labs remained elevated throughout the duration of his stay, with few exceptions. Around the time of his admission, the patient’s renal profile was fairly stable but began to decline near the latter end of his stay. In addition, the patient had very low albumin levels which ranged from 1.6 to 2.0 gm/dL. In general, inflammatory processes are inversely correlated to serum albumin levels and, as a result, the serum protein can be utilized as an indicator of morbidity, mortality, and the severity of an illness (Charney & Malone, 2009). Labs were not draw, however, for C-reactive protein which is used to monitor the intensity of an inflammatory process. Prealbumin was not tested for either which can, in conjunction with other tests, indicate malnutrition to a degree. The patient’s lactate level was elevated, indicating lactic acidosis likely due to oxygen depletion in the blood. Labs indicating anemia steadily worsened throughout the patient’s stay.Since the patient was intubated and sedated while in the hospital, a personal account of his diet history was unable to be obtained. Likewise, the nursing staff knew little about the patient’s dietary habits prior to admission, and little was provided concerning them in the medical record. However, the wife, who is separated from her husband and living in a different city, was contacted and able to provide some information. She claimed that the patient had lost weight prior to admission by consuming smaller, more frequent meals comprised mainly of fruits and vegetables. However, she could not provide details on what constituted a small meal for the patient. She also stated that food shopping and preparation was done by the patient’s brother and sister since he was unable to do so himself due to his morbid obesity. After the initial dietitian assessment of the patient, the PSU(2010) was utilized to determine that he needed approximately 3,229 kcal/d to meet his metabolic demands. However, the patient’s needs were even higher since he was under sixty years of age. Therefore, his need should have been calculated using the PSU(2003b). Protein needs were estimated to be approximately 170 g/d or 2.5 g/kg IBW due to his class III, morbidly obese status. Fluid needs were estimated at approximately 3,300 mL/d, based on the 1 mL/kcal method. The patient was assigned a level three nutritional compromise status throughout his hospital stay which entailed a reassessment every five days (reassessments occurred earlier if the patient’s follow-up date fell on the weekend). The overall severity of his condition and the need to monitor his enteral feedings warranted such frequent nutrition assessments.Nutrition Diagnoses, Nutrition Interventions, & Monitoring & EvaluationThe patient was evaluated by a dietitian (and/or dietetic intern) seven times during his twenty-four day hospital stay and assigned a total of three nutrition diagnoses including excessive fat intake, inadequate energy intake, and altered gastrointestinal (GI) function. The first consult was ordered by the physician for tube feeding recommendations one day after the patient was admitted. At the time, the patient was receiving 81 mL/hr of Diprivan which provided 2,138 kcal from fat. As a result, the PES statement was as follows: excessive fat intake related to current dose of lipids from Diprivan as evidenced by parenteral intake of greater than 200 g/d of lipids and a high triglyceride level. The nutrition intervention consisted of recommending Glucerna 1.5 Cal? tube feeing at a goal rate of 80 ml/hr once the patient was weaned from Diprivan to provide 2,880 kcal, 158 g protein, and 1,457 mL fluid (tube feeding fluid supplemented intravenous fluid administered to the patient). The tube feeding recommendation was calculated to provide 89% of his estimated caloric needs. If the patient had tolerated the feeding, the tube feeding goal rate would have increased. Evaluation of the response to the nutrition intervention consisted of monitoring the patient’s tolerance to the tube feeding, promoting weight loss, normalizing blood glucose and triglyceride levels, and promoting surgical wound healing (patient had underwent surgical debridement of groin abscess). When the patient was seen for the second time, his diet order was Jevity 1.5 Cal? at 50 mL/hr which provided 1,800 kcal, 77 g protein, and 912 mL fluid. Due to the patient receiving only 56% of his estimated energy needs, the resultant PES statement was as follows: inadequate energy intake related to current tube feeding order as evidenced by intake record. One nutrition intervention consisted of recommending Glucerna 1.5 Cal? at 80 mL/hr again to provide adequate nutrition and better control for blood glucose levels. Another intervention was the recommendation of a phosphate binder to better control blood phosphate levels. Monitoring and evaluation of the interventions consisted of maintaining the patient’s lean body mass while promoting weight loss, normalizing blood glucose levels, promoting the trend of electrolytes toward normal limits, and promoting surgical wound healing.For the third, fourth, and fifth time the patient was seen, no new dietary interventions were introduced. The patient was still receiving Jevity 1.5 Cal? at 50 mL/hr and was later made NPO for a gastrograph study in preparation for a PEG tube placement. Monitoring and evaluation of the interventions remained the same.When the patient was assessed for the sixth time, he had been NPO for two days due to excessive gastric residuals and vomiting. As a result, the following PES statement was utilized: altered GI function related to lack of GI motility due to physical inactivity, possible inadequate head of bed elevation, and maximum dose of Levophed as evidenced by vomiting, excessive residuals, and a NPO diet. The nutrition intervention consisted of recommendations for bowel rest and the possible initiation of peripheral parenteral nutrition (PPN) if deemed medically appropriate. More specifically, Clinimix 2.75/5 at 100 mL/hr was suggested to provide 2,400 kcal and 66 g protein. If the Levophed dose began trending below 20 mcg/min consistently, then enteral nutrition with a fiber-free formula was recommended to be reinitiated. Monitoring and evaluation remained mostly the same with the addition of ensuring proper hydration to prevent dehydration or overhydration. On the final day the patient was assessed, he was assigned the following PES statement: altered GI function related to possible ischemic bowel disease as evidenced by a high lactate level. X-ray exams of the patient’s abdomen could not clearly indicate ischemic bowel disease due to his morbid obesity. Despite this, the patient was placed on total parenteral nutrition (TPN) which was managed by his renal physician. The dietitian recommended that the TPN provide at least 70 to 80% of the patient’s estimated energy needs with a goal of 170 g amino acids, 350 g dextrose, and 50 g intralipids. A recommendation was made to monitor the patient for refeeding syndrome since he had been NPO for four days and had, before that, been underfed with the tube feedings. Monitoring and evaluation consisted of the patient meeting at least 70% of his goal nutritional needs, improving his acid-base, electrolyte, and glucose profile, and promoting surgical wound healing. Conclusion The patient was admitted to the hospital to undergo surgical debridement of a right groin abscess. However, during his hospitalization he developed a plethora of other conditions. While the patient was medically diagnosed with morbid obesity, DM, ARF, cellulitis, UTI, septic shock, AKI, and possible ischemic bowel disease, he was nutritionally diagnosed with excessive fat intake, inadequate energy intake, and altered GI function. Nutrition interventions focused on recommending a tube feeding with a goal rate, a phosphate binder, initiation of PPN and later TPN. Recommendations for the tube feeding were not implemented nor was the recommendation to administer a phosphate binder to the patient. TPN rather than PPN was initiated by the physician to provide for the patient nutritionally. However, the amount of nutrients delivered by the TPN was not notated in the electronic medical record. Despite the maximal medical therapy provided to the patient, his clinical response remained dismal. As a result, the family agreed to withdrawal of care and the patient was subsequently discharged to hospice. The patient was then taken off the ventilator and died shortly thereafter. Review of Key PointsA recent study by Sturm & Hattori (2013) found that morbid obesity affects approximately 6.6% of adult Americans. With morbid obesity, physiological changes occur in relation to the hormones involved in appetite regulation and weight management, thereby altering the normal functioning of the neuroendocrine system. Severe obesity is also associated with many comorbid conditions, including type II DM, CAD, and sleep apnea as well as various cancers. Likewise, many different factors contribute to the etiology of morbid obesity such as diet, physical activity level, sleep deprivation, heredity, obesogens, and pathogens. Several treatment modalities are available for the management of morbid obesity, including lifestyle modifications, pharmaceutical management, and surgical interventions. Nutrition interventions focus on decreasing caloric intake in order to create a negative energy balance, thereby causing weight loss. In critically ill, morbidly obese individuals, the Penn State University predictive equations should be utilized to determine RMR. While morbid obesity is not a leading cause of death in the United States, it does increase an individual’s risk for developing related comorbidities. Some of these comorbidities, however, do constitute leading causes of death in the United States, including CAD, stroke, DM, and cancer. Personal ImpressionsOne impression that I had pertained to the lack of receptivity on the part of some clinical staff members to dietary recommendations. Several consults were sent to the dietitians to assess the patient’s nutritional needs. Once dietary recommendations were provided, however, they were not always adhered to. While I understand that most decisions pertaining to the patient’s care are ultimately made by the physician, I felt as though evidence-based guidelines concerning nutrition were not implemented. Another impression I had pertained to the delicacy with which I perceived I needed to ask questions with. For example, the medical record contained little information pertaining to the patient’s diet history, weight history, and social history. Similarly, the nursing staff I spoke with was unaware of the details related to these topics. Fortunately, however, I ran into the patient’s wife, who was separated from her husband, during patient rounding in the medical ICU. I proceeded to ask her questions related to the patient’s diet and weight history so that I could more accurately understand and assess the patient nutritionally. However, in the process of doing so, I felt that my questions might be regarded by the wife as irrelevant or unnecessary due to the gravity of the medical condition that the patient was currently in. Thankfully the wife was very helpful and willing to provide as much information as she could related to these topics. In the end, I realized that my uncomfortableness in such a situation was unwarranted, but it helped to emphasize the importance of being sensitive and tactful with family members, especially during such difficult times.The patient was admitted to the hospital to undergo a relatively simple surgical procedure but ended up developing several complications afterwards. Despite all the diligent and dedicated effort on the part of the medical staff, the patient ended up dying. 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