Intensive Care Management, Sepsis, and Systemic Inflammatory Response Syndrome in the Bariatric Patient

| January 1, 2015

by Vivek Bindal, MS, FNB, and Ranjan Sudan, MD

Bariatric Times. 2015;12(1):10–14.

Objective: To review the current literature on pathophysiology and challenges in management of the critically ill bariatric patient population.
Design: A PubMed search was conducted from 2000 to 2014. Key words used included “intensive care,” “bariatric surgery,” and “morbid obesity.”
Results: Patients with morbid obesity have a higher incidence of obstructive sleep apnea, obesity hypoventilation syndrome, venous thromboembolism, aspiration, and intra-abdominal hypertension. These, along with other comorbidities, lead to challenges in airway and pulmonary management, maintaining nutrition, and in dosing medications appropriately. Obesity is also associated with chronic inflammation, hypercoagulability, and insulin resistance, contributing to aberrant physiological responses.
Conclusions: Morbid obesity is associated with a chronic inflammatory state and critically ill bariatric patients pose distinct challenges to the intensive care team. In order to optimally manage these patients, the entire team has to be well versed in the pathophysiology of obese patients, and the special risks and difficulties that might be encountered.

Morbid obesity is associated with an increased incidence of comorbidities like type 2 diabetes mellitus (T2DM), hypertension (HTN), obstructive sleep apnea (OSA), non-alcoholic steato-hepatitis (NASH), and coronary artery disease (CAD). These comorbidities can be treated very effectively and consistently by bariatric surgery, resulting in improved quality of life and survival.[1] Although the safety profile of bariatric surgery has improved greatly over the last several years, patients who undergo bariatric surgery are higher risk patients, especially those with male gender, age more than 50 years, body mass index (BMI) more than 60kg/m2 and intra-operative complications.[2] If patients undergoing bariatric surgery develop a complication, they may require intensive care management. This article details the pathophysiology of obesity, sepsis, and management of the various unique aspects of bariatric patients and differentiates them from the general patient population in the intensive care unit (ICU).

Pathophysiology of Obesity
Obesity is associated with insulin resistance (IR) and greatly increases the risk of developing T2DM in some individuals. IR is manifested by a failure of insulin to inhibit gluconeogenesis by the liver and a diminished glucose uptake in response to insulin by skeletal muscle and adipose tissue.[3] In addition, obesity is a state of chronic low-grade inflammation with increased levels of inflammatory markers, such as C-reactive protein (CRP), interleukin (IL)-6 and tumor necrosis factor (TNF) α.[4] In severe obesity, adipokine overexpression and chronic microinflammation is seen and correlates with atherosclerosis, arterial hypertension, endothelial dysfunction, increased blood viscosity, insulin resistance, and various stigmata of metabolic syndrome.[5]

Human adipose tissue is divided into visceral adipose tissue (VAT) and subcutaneous adipose tissues (SAT). The VAT is implicated to a greater extent in obesity associated chronic inflammation. The term adipokines or adipocytokines has been used for small molecule proteins that are produced and secreted by the white adipose tissue. Some of these molecules are exclusively produced by the adipose tissue. These include leptin and adiponectin, and others, such as CRP, TNF α , IL-6, IL-1, IL-10, IL-18. Serum amyloid protein are produced in abundance not only by adipose tissue but also by other organs such as liver, skeletal muscle, and immune cells. Obesity is associated with a moderate and chronic increase in such inflammatory molecules, with the exception of adiponectin, which is decreased in obesity.[4]

In obesity, there is also increased infiltration of macrophages in the adipose tissue. Although local pre-adipocytes can convert themselves into macrophages, this increase in macrophages in the adipose tissue is believed to be primarily due to increased infiltration. One of the causes for macrophage infiltration may be bursting of the adipocytes, which releases intracellular chemokines. Further, leptin is known to cause increased secretion of macrophage chemo attractant molecules. The increased free fatty acids in obesity can also activate the macrophages through toll like receptor 4.[6] Plasma level of chimerin, another macrophage chemo-attractant protein, has been shown to be elevated in the obese state and decreased after bariatric surgery.[7]

Obesity is also a hypercoagulable state. Plasminogen activator inhibitor 1 (PAI-1) is the primary physiological inhibitor of plasminogen activation in vivo. Production of PAI-1 by adipose tissue, in particular by omental fat, could be responsible for the elevated plasma PAI-1 level observed in insulin resistance.[8] Circulating PAI-1 levels are also elevated in patients with coronary heart disease and may play an important role in the development of atherothrombosis by decreasing fibrin degradation.

In summary, obesity is associated with insulin resistance, chronic inflammation, and hypercoagulability, contributing to various comorbidities and altered physiological responses.
Physiological effects of obesity on major organ systems. Obesity affects physiological function of almost all organ systems in the body. These changes in turn dictate management in the critically ill patient with morbid obesity.

Cardiovascular. In obesity, increased blood volume, cardiac output, and vascular tone are seen and decreased ventricular contractility can lead to ventricular dilation (obesity cardiomyopathy).[9]

Respiratory. Pulmonary and chest wall compliance is reduced, and there is elevated airway resistance and ventilation/perfusion mismatch. This leads to decreased functional residual capacity and vital capacity.[10]

Renal. Glomerular filtration rate is increased leading to increased clearance of drugs excreted by kidneys. However, obesity associated comorbidities like T2DM and HTN may lead to nephropathy and decreased renal function in many patients.

Gastrointestinal. Incidence of hiatal hernia is increased as is volume of gastric secretion resulting in pH reduction and the chances of pulmonary aspiration is increased.

Intensive Care Unit Outcomes
It is commonly believed that obesity is associated with poor ICU outcomes, but the current evidence fails to establish this consistently. Some published studies have shown obesity to be protective during critical illness; whereas, others have shown a negative or equivocal effect.[11–13] A recent meta-analysis of 14 studies with more than 15,000 patients with obesity (BMI>30kg/m2) in medical and surgical ICUs showed no significant difference in mortality for patients with obesity compared to normal weight patients. However, length of stay and days requiring mechanical ventilation were increased. In a subgroup analysis of patients with moderate obesity (BMI 30kg/m2–40kg/m2), a highly significant increase in ICU-survival rate was found among these patients compared with normal-weight patients.[14]

Common Challenges in Bariatric Surgery Patients in the Intensive Care Unit
The comorbidities associated with obesity pose additional challenges in the critical care management of these severely ill patients as compared to the general ICU patient pool.

Obstructive sleep apnea. Obesity is strongly associated with OSA, a condition in which recurrent episodes of upper airway obstruction during sleep are associated with arterial oxygen desaturation and repetitive arousals resulting in disrupted sleep and excessive daytime sleepiness. OSA is a clinical indicator of a ‘‘difficult airway’’ and can contribute to the development of respiratory failure resulting in failed extubation following mechanical ventilation15 and thereby increasing the risk of ICU admission.

Obesity hypoventilation syndrome. Obesity hypoventilation syndrome (OHS) is hypercapnia (arterial carbon dioxide tension [PaCO2] >45mm Hg [6 kPa]) during wakefulness associated with obesity (BMI>30kg/m2) in the absence of other known causes of alveolar hypoventilation.[16] The prevalence of OHS increases as BMI increases, and up to 31 percent of hospitalized patients with BMI>35kg/m2 have hypercapnia without any other cause.[17] Therefore, the medical team must be aware of the significant role of sleep-related hypoventilation in the patient with obesity to avoid failure to wean from ventilatory support or to prevent reintubation due to recurrent respiratory failure.[15] In patients with OSA, extubation can be considered once ventilatory capacity during the awake state is adequate; however, ongoing noninvasive ventilation (NIV) may be required during sleep.[18]

Airway management. Intubation can be quite difficult in individuals with morbid obesity. Proper patient positioning is of utmost importance. Awake intubation is preferred by many anesthesiologists.[19] Laryngeal mask airway is effective and provides a conduit for the bronchoscope. In some patients, fiber optic guidance or video-assisted intubation may be required. A surgical tracheostomy, if needed, may be difficult to perform and usually requires longer tracheostomy tubes (e.g., Bivona®, Smiths Medical, London, England).

Pulmonary management. A review of nearly 25,000 patients in the post-anesthesia care unit found that patients with obesity have twice the rate of critical respiratory events (e.g., upper airway obstruction, hypoventilation, unforeseen hypoxemia) requiring emergent management after extubation than non-obese patients.[20] There is increased chest wall resistance, increased airway resistance, and an abnormally high diaphragm. Because the lung volumes are decreased and airway resistance is increased, the tidal volume is calculated based on ideal body weight (IBW [6mL/kg]).[21] Reverse Trendelenburg position at 45 degrees helps in extubation. Continuous positive airway pressure (CPAP) and incentive spirometry are useful to prevent or treat postoperative atelectasis.[22] Sudden postoperative respiratory decompensation may also indicate either pulmonary embolism or the onset of systemic inflammatory response syndrome (SIRS)/sepsis due to an anastomotic leak.

Venous thromboembolism. Patients undergoing bariatric surgery are at increased risk for venous thromboembolism (VTE).[23] Therefore, in the modern era, the majority of bariatric surgery programs have instituted protocols for VTE prophylaxis. The incidence of symptomatic deep venous thrombosis (DVT) and pulmonary embolism (PE) ranges from 0 to 5.4 percent and 0 to 6.4 percent, respectively.[24] However, most large series report VTE rates less than one percent for the average risk in patients undergoing bariatric surgery. These are comparable to the rates of VTE for many other elective operations performed today.[24]

The ideal method of prophylaxis for VTE complications in bariatric surgery has yet to be determined. Patients undergoing bariatric surgery are considered to be at moderate to high risk of having thrombo-embolic complications. There is a wide variation in the published literature on optimal guidelines for the prevention of perioperative VTE events. The most accepted forms of prophylaxis range from mechanical compression devices with early ambulation alone to the addition of chemoprophylaxis and the use of inferior vena cava (IVC) filters. For chemoprophylaxis, unfractionated heparin (UFH) and low molecular weight heparin (LMWH) have been used extensively in bariatric patients. A systematic review that included 30 publications of open and laparoscopic bariatric procedures reported various combinations of UFH and LMWH with or without mechanical prophylaxis and IVC filters.[25] The authors concluded that it is reasonable to use UFH 5000 IU subcutaneously or LMWH (30 to 40mg) starting before surgery and continuing UFH every 8 hours or LMWH every 12 to 24 hours after surgery in combination with sequential compression devices.[25]

Pulmonary aspiration. There is an increased risk of aspiration in patients with morbid obesity. Changes in gastroesophageal anatomy and physiology caused by obesity may explain this association. These changes include an increased prevalence of esophageal motor disorders, diminished lower esophageal sphincter (LES) pressure, the development of a hiatal hernia, and increased intra-gastric pressure. Central adiposity may be the most important risk for the development of reflux and related complications, such as Barrett’s esophagus and esophageal adenocarcinoma.[26]

The use of narcotic analgesics and other drugs that alter intestinal motility may increase the risk of reflux and complications of aspiration in patients with obesity. H2 antagonists and proton pump inhibitors, which increase gastric pH and decrease the volume of gastric secretions might minimize the deleterious effects of gastric acid aspiration on the lung, but the loss of the anti-microbial effects of gastric acid has been suggested as a potential risk factor for pneumonia. Elevation of the patient’s head may decrease intra-abdominal pressure and reduce the risk for aspiration after intubation.[27]
Intra-abdominal hypertension. Studies show that patients with obesity have a higher intra-abdominal pressure than non-obese subjects. In both the non-obese and obese critically ill patient, elevated intra-abdominal pressure in the patient can have far-reaching deleterious effects on end-organ function. Individuals with morbid obesity are at a greater risk of developing abdominal compartment syndrome because of pre-existing baseline intra-abdominal hypertension (IAH) and organ dysfunction. Clinicians should have a low threshold for monitoring intra-abdominal pressure in patients with obesity.[28]

Disease processes that are common in patients with morbid obesity, such as OHS, pseudotumor cerebri, gastroesophageal reflux disease (GERD), and stress urinary incontinence are now being recognized as conditions caused by the increased intra-abdominal pressure occurring in patients with an elevated BMI. Also, the increased incidence of poor fascial healing and incisional hernia rates has been related to the IAH-induced reductions in blood flow in the rectus sheath and abdominal wall. IAH-related complications of morbid obesity generally respond to weight loss.

Anastomotic Leak/SIRS/Sepsis
Anastomotic leak is a dreaded and severe complication of any bariatric procedure. It is one of the common causes of ICU admission after bariatric surgery. It can lead to SIRS and sepsis. Sepsis is a leading cause of morbidity and mortality and is 10 times more common than perioperative myocardial infarction and VTE. Septic shock has a mortality rate of 30 percent among elective general surgical patients and rate of 39 percent among emergent surgical patients. Risk factors include age older than 60 years, the need for emergency surgery, and the presence of comorbid conditions.
Hamilton et al[29] described the following alarming signs indicating an anastomotic leak:
•    Tachycardia (heart rate > 120 beats per minute [bpm])
•    SaO2 < 92 percent (on room air)
•    Respiratory rate > 24 breaths/minute.

The abdominal signs of peritonitis in patients with morbid obesity are not very reliable and may be difficult to elicit because of a thick layer of abdominal fat. Computed tomography (CT) scan or an upper gastrointestinal series may aid in diagnosing a leak. In the event of a leak, the cornerstone of treatment is source control to limit the degree of peritoneal contamination. Stable patients in whom the leak is contained are often treated by percutaneous placement of drains and providing parenteral nutrition. Diagnostic laparoscopy or laparotomy is often performed if the leak is not contained or the patient is septic. Surgical intervention should be performed with a low threshold with the aim of controlling the leak by placing adequate drains and repairing the leaking segment, if possible, depending on tissue integrity.
Systemic inflammatory response syndrome and sepsis. SIRS is defined by presence of two or more of the following criteria:[30]
•    Body temperature below 36°C or above 38°C
•    Heart rate greater than 90 bpm
•    Tachypnea, with > 20 breaths per minute, or a PaCO2 of less than 32 mm Hg
•    White blood cell (WBC) count less than 4,000 cells/microliter or greater than 12,000 cells/microliter or the presence > 10 percent bands.

Sepsis is defined as SIRS with an infection requiring surgical intervention for source control or an infection within 14 days of a major surgical procedure.

Severe sepsis is defined using the following criteria:
•    SIRS + infection + acute organ dysfunction
•    Glasgow Coma Score (GCS) less than 13
•    PaO2: FIO2 ratio < 250
•    Urine output < 0.5mL/kg for one hour or increase in serum creatinine 0.5mg/dL or more from baseline despite adequate volume resuscitation
•    International normalized ratio (INR) > 1.5, platelet count < 80,000/mL
•    Hypoperfusion: lactate level > 4mmol/L.

Septic shock is defined as SIRS with an infection and acute cardiac dysfunction. Cardiac dysfunction must meet both of the following criteria:
•    Adequate fluid resuscitation: intravenous (IV) fluid challenge ≥20mL/kg/IBW of isotonic crystalloid infusion or central venous pressure (CVP) ≥ to 8 mm Hg or pulmonary capillary wedge pressure (PCWP) ≥ 12 mm Hg
•    Require vasopressors to increase mean arterial pressure (MAP) to ≥ 65 mm Hg.

All efforts should be undertaken to identify sepsis early in its course so as to enable timely action. Some of the early indicators of sepsis include oliguria, acute hypoxia, and altered mental status; however, these may mistakenly be attributed to other etiologies. Oliguria is often attributed to under-resuscitation in the operating room or volume loss from the gastrointestinal tract or bleeding. Altered mental status is often thought to be due to narcotic administration or ICU psychosis, and acute hypoxia due to pulmonary embolism.

Resuscitation involves restoring intravascular volume, diagnosing the source of infection, and initiating broad-spectrum antimicrobial therapy and source control.

Tissue hypoperfusion. Signs of tissue hypoperfusion should prompt aggressive resuscitative measures. If a patient develops signs of sepsis with tissue hypoperfusion, it indicates severe sepsis or a septic shock. Tissue hypoperfusion is indicated by the following:
•    Urine output < 0.5 mL/kg of IBW
•    MAP < 65 mm Hg
•    GCS score < than 12
•    Serum lactate ≥ 4 mmol/L.

Fluid resuscitation. To administer adequate fluids in the desired time, a large-bore peripheral IV line should be established as soon as possible. If peripheral access is not attainable, a central venous line should be inserted in a timely fashion.
The initial fluid challenge should be 1,000 cc of crystalloid over 30 minutes. When colloids are given, the initial fluid bolus should be 300 to 500mL over 30 minutes. Additional fluids are given based on the patient’s response. A baseline serum lactate should be sent when sepsis is identified.
The goals of resuscitation are as follows:
•    Target CVP of 8 to 12 mm Hg in non-intubated patients and a target CVP of 12 to 15 mm Hg in mechanically ventilated patients
•    MAP of 65 mm Hg or greater
•    Urine output of 0.5 mL/kg/hour or greater
•    Central venous oxygen saturation (ScvO2) of ≥ 70 percent or mixed venous oxygen saturation (SvO2) of ≥ 65 percent
•    If MAP of 65 to 90mm is not achieved with restoration of intravascular volume with crystalloids or colloids, red blood cells are transfused to achieve hematocrit of ≥ 30 percent.

The goals of resuscitation should be achieved within six hours of the recognition of sepsis.

Early goal-directed therapy. Early goal-directed therapy (EGDT) was introduced by Emanuel P. Rivers in 2001,[31] and when provided at the earliest stages of severe sepsis and septic shock, has been shown to have significant short-term and long-term benefits and improve survival in critically ill patients. These benefits arise from the early identification of patients who are at high risk for cardiovascular collapse and from early therapeutic intervention to restore a balance between oxygen delivery and oxygen demand. The protocol involves monitoring tissue perfusion by measuring SvO2, ScvO2, or peripheral muscle hemoglobin oxygen saturation (StO2).

Vasopressors. Septic shock is a vasodilatory shock with a high cardiac output and low systemic vascular resistance. Therefore, restoration of vascular tone is a target. Both norepinephrine and dopamine are acceptable first-line agents for treatment of septic shock. Dopamine increases cardiac output and at higher doses (>7.5mg/kg/minute) results in vasoconstriction. In those patients who are refractory to first-line vasopressors, vasopressin may be beneficial.

Antimicrobial management. Broad spectrum antibiotics are started early in the course of sepsis. A minimum of two blood cultures should be obtained; one blood culture from each vascular access device and one blood culture from a peripheral puncture. Additional cultures from other sites (respiratory system, urinary tract, drain) are also taken. Radiographic imaging is used to identify any undrained abscess or fluid collection.

Activated protein C. Activated protein C (APC) is a major anticoagulant factor. It is activated by the binding of thrombin to thrombomodulin on the surface of the endothelium. Once activated, protein C directly inhibits the clotting cascade. In patients with severe sepsis and septic shock, production of APC is decreased. This causes shift towards the pro-coagulant state resulting in microvascular thrombosis, tissue hypoxia, and direct tissue damage, which ultimately results in organ dysfunction or failure. Therefore, administration of APC was thought to be a means of reversing the pro-coagulant state seen in severe sepsis and septic shock;[32] however, it was withdrawn from the market after studies revealed that there was no benefit of using APC compared to a placebo.[33]

Special Considerations in Critical Care of Bariatric Patients

Drug dosing. Obesity affects the pharmacokinetics of drugs because of the following changes:
•    Increased glomerular filtration rate (GFR)
•    T2DM/HTN adversely affecting kidney function
•    Liver pathology (NASH/Cirrhosis)
•    Increased blood volume
•    Accumulation of lipophilic drugs in adipose tissue.

Volume of distribution of relatively hydrophilic drugs correlates well with IBW, with correlation coefficients of up to 0.9. IBW can be used to accurately predict the loading dose required for these drugs to attain a target peak plasma concentration. For lipophilic drugs, volume of distribution correlates better with actual body weight (ABW) than with IBW.[34] For instance; vancomycin is a lipophilic drug and is administered using ABW, while opioids and benzodiazepines are hydrophilic drugs and are administered using IBW. Some drugs like aminoglycosides and fluoroquinolones are administered using adjusted body weight [IBW + 0.4 (ABW–IBW)] to account for a larger volume of distribution in patients with obesity.

Nutritional assessment. The initial assessment of the critically ill patient should include anthropometric measures (ABW, IBW, BMI, waist circumference) and biomarkers of metabolic syndrome (serum triglycerides, cholesterol, glucose). Protein and calorie requirement should be determined to set the goals of nutrition therapy. Caloric requirements can be measured by either indirect calorimetry or by predictive equations (Penn State/Ireton-Jones/Mifflin) or can be based on IBW. Protein requirements are simpler to calculate based on IBW, aided by 24 hour urine urea nitrogen (UUN). Protein requirements may be estimated by >2.0g/kg IBW/day for Class I and II obesity and by >2.5g/kg IBW/d for Class III obesity.[35]

High protein hypocaloric feed. Enteral feeding is preferred and may be administered using a nasogastric, gastric, or jejunal feeding tube. Post-pyloric delivery of feed is preferred to prevent gastroesophageal reflux and aspiration because of increased intra-gastric pressure in patients with obesity. The requirements for a high protein hypocaloric feed are calculated using IBW as follows:[35]
•    2.0g/kg/d protein for Class I and II obesity
•    2.5g/kg/d protein for Class III obesity
•    20–25kcal/kg IBW/d, or 11–14 kcal/kg ABW/d.

Optimal enteral feed. For optimal enteral feeding, a minimum of 125g of glucose per day should be given. For patients with healing wounds, it should be increased to 250g/day. The caloric density should be less than 1.0kcal/mL and 15 to 20 percent of calories should come from fat. Various immune modulating nutrients should be considered for administration to these patients like L-arginine, Leucine, L-carnitine, magnesium, zinc, fish oil and α-lipoic acid.

The critically ill patients with morbid obesity may be potentially deficient in micronutrients like iron, folate, vitamin B12, copper, thiamine, vitamins D, A, E, K, and essential fatty acids. Deficiencies of these minerals and vitamins should be assessed and treated promptly.

Morbid obesity is a chronic inflammatory state and critically ill bariatric patients pose distinct challenges to the intensive care team. There are a host of factors to take into account while managing these patients, especially after bariatric surgery. The entire team has to be well versed in the pathophysiology of obesity and the special risks and difficulties in managing these patients. These patients have a narrow window of opportunity and the right decision can make all the difference in eventual outcome; therefore, better evidence-based guidelines for management of this precarious population are needed.

1.    Sjostrom L, Lindroos AK, Peltonen M, et al. Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. N Engl J Med. 2004;351(26):2683–2693.
2.    Helling TS, Willoughby TL, Maxfield DM, Ryan P. Determinants of the need for intensive care and prolonged mechanical ventilation in patients undergoing bariatric surgery. Obes Surg. 2004;14(8):1036–1041.
3.    Reaven GM. Importance of identifying the overweight patient who will benefit the most by losing weight. Ann Intern Med. 2003;138(5):420–423.
4.    Rao SR. Inflammatory markers and bariatric surgery: a meta-analysis. Inflamm Res. 2012;61(8):789–807. Epub 2012 May 16.
5.    Herbert A, Liu C, Karamohamed S, et al. BMI modifies associations of IL-6 genotypes with insulin resistance: the Framingham Study. Obesity (Silver Spring). 2006;14(8):1454–1461.
6.    Shi H, Kokoeva MV, Inouye K, et al. TLR4 links innate immunity and fatty acid-induced insulin resistance. J Clin Invest. 2006;116(11):3015–3025. Epub 2006 Oct 19.
7.    Ress C, Tschoner A, Engl J, Klaus A, Tilg H, Ebenbichler CF, et al. Effect of bariatric surgery on circulating chemerin levels. Eur J Clin Invest. 2010;40(3):277–280.
8.    Juhan-Vague I, Alessi MC, Morange PE. Hypofibrinolysis and increased PAI-1 are linked to atherothrombosis via insulin resistance and obesity. Ann Med. 2000;32 Suppl 1:78–84.
9.    Alpert MA. Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome. Am J Med Sci. 2001;321(4):225–236.
10.    Pieracci FM, Barie PS, Pomp A. Critical care of the bariatric patient. Crit Care Med. 2006;34(6):1796–1804.
11.    Goulenok C, Monchi M, Chiche JD, et al. Influence of overweight on ICU mortality: a prospective study. Chest. 2004;125(4):1441-5.
12.    Diaz JJ Jr, Norris PR, Collier BR, et al. Morbid obesity is not a risk factor for mortality in critically ill trauma patients. J Trauma. 2009;66(1):226–231.
13.    Frat JP, Gissot V, Ragot S, et al. Impact of obesity in mechanically ventilated patients: a prospective study. Intensive Care Med. 2008;34(11):1991–1998.
14.    Akinnusi ME, Pineda LA, El Solh AA. Effect of obesity on intensive care morbidity and mortality: a meta-analysis. Crit Care Med. 2008;36(1):151–158.
15.    Malhotra A, Hillman D. Obesity and the lung: 3. Obesity, respiration and intensive care. Thorax. 2008;63(10):925–931
16.    Olson AL, Zwillich C. The obesity hypoventilation syndrome. Am J Med. 2005;118(9):948–956.
17.    Nowbar S, Burkart KM, Gonzales R, et al. Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome. Am J Med. 2004;116(1):1–7.
18.    El-Solh AA, Aquilina A, Pineda L, Dhanvantri V, Grant B, Bouquin P. Noninvasive ventilation for prevention of post-extubation respiratory failure in obese patients. Eur Respir J. 2006;28(3):588–595. Epub 2006 May 31.
19.    Levitan R, Ochroch EA. Airway management and direct laryngoscopy. A review and update. Crit Care Clin. 2000;16(3):373–388, v.
20.    Rose DK, Cohen MM, Wigglesworth DF, DeBoer DP. Critical respiratory events in the postanesthesia care unit. Patient, surgical, and anesthetic factors. Anesthesiology. 1994;81(2):410–418.
21.    El-Solh AA. Clinical approach to the critically ill, morbidly obese patient. Am J Respir Crit Care Med. 2004;169(5):557–561.
22.    Pelosi P, Ravagnan I, Giurati G, et al. Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. Anesthesiology. 1999;91(5):1221–1231.
23.    Stein PD, Goldman J. Obesity and thromboembolic disease. Clin Chest Med. 2009;30(3):489–493, viii.
24.    American Society for M, Bariatric Surgery Clinical Issues C. ASMBS updated position statement on prophylactic measures to reduce the risk of venous thromboembolism in bariatric surgery patients. Surg Obes Relat Dis. 2013;9(4):493–497.
25.    Agarwal R, Hecht TE, Lazo MC, Umscheid CA. Venous thromboembolism prophylaxis for patients undergoing bariatric surgery: a systematic review. Surg Obes Relat Dis. 2010;6(2):213–220.
26.    Friedenberg FK, Xanthopoulos M, Foster GD, Richter JE. The association between gastroesophageal reflux disease and obesity. Am J Gastroenterol. 2008;103(8):2111–2122.
27.    Honiden S, McArdle JR. Obesity in the intensive care unit. Clin Chest Med. 2009;30(3):581–599, x.
28.    Malbrain ML, De laet IE. Intra-abdominal hypertension: evolving concepts. Clin Chest Med. 2009;30(1):45–70, viii.
29.    Hamilton EC, Sims TL, Hamilton TT, Mullican MA, Jones DB, Provost DA. Clinical predictors of leak after laparoscopic Roux-en-Y gastric bypass for morbid obesity. Surg Endosc. 2003;17(5):679–684. Epub 2003 Mar 7.
30.    Buckman S, Orr PJ, Agarwal S. Sepsis, severe sepsis, and septic shock. In: Souba WW (ed). ACS Surgery: Principles & Practice. 6th ed. New York, New York: WebMD Professional Pub.; 2007: 1952.
31.    Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368–1377.
32.    Levy H, Small D, Heiselman DE, et al. Obesity does not alter the pharmacokinetics of drotrecogin alfa (activated) in severe sepsis. Ann Pharmacother. 2005;39(2):262–267. Epub 2005 Jan 4.
33.    Marti-Carvajal AJ, Sola I, Gluud C, Lathyris D, Cardona AF. Human recombinant protein C for severe sepsis and septic shock in adult and paediatric patients. Cochrane Database Syst Rev. 2012;12:CD004388.
34.    Morgan DJ, Bray KM. Lean body mass as a predictor of drug dosage. Implications for drug therapy. Clin Pharmacokinet. 1994;26(4):292–307.
35.    McClave SA, Kushner R, Van Way CW, et al. Nutrition therapy of the severely obese, critically ill patient: summation of conclusions and recommendations. JPEN J Parenter Enteral Nutr. 2011;35(5 Suppl):88S–96S.

Author Affiliation: Drs. Bindal and Sudan are from Duke University Medical Center, Durham, North Carolina.

Funding: No funding was provided.

Disclosures: The authors report no conflicts relevant to the content of this article.

Tags: , , , , , , ,

Category: Past Articles, Review

Comments are closed.