By William H. Thompson, MD

Associate Professor of Medicine, University of Washington, Seattle

Dr. Thompson reports no financial relationships relevant to this field of study.

Obesity is a growing epidemic that affects the health of millions of Americans and will require healthcare systems to anticipate growth in the numbers of obese patients. The National Institutes of Health and World Health Organization classify body mass index (BMI) in kg/m2 as overweight (25.0-29.9), class I obesity (30.0-34.9), class II obesity (35.0-39.9), and class III or extreme obesity (> 40.0).1 BMIs of > 40.0 and > 50.0 have been classified previously as morbid obesity and super morbid obesity, respectively.2 Trends in obesity based on the National Health and Nutrition Examination Survey (NHANES) suggest an increase in age-adjusted prevalence of obesity in the United States from 33.7% in 2007-2008 to 39.6% in 2015-2016.3 Given that obesity carries with it an increased risk of medical conditions that can result in an intensive care unit (ICU) admission (e.g., coronary artery disease, diabetes, stroke, pulmonary embolism),4 the prevalence of obesity in those admitted to the ICU also has risen, with rates varying from approximately 20% to 36.5%.5,6 With the growth in the numbers of patients undergoing bariatric surgery (252,000 U.S. and Canadian cases in 2018),7 more patients are being treated in the ICU for complications of that procedure. In addition, obesity is an independent risk factor for mortality in the ICU.8 This article will highlight some important practical aspects of care that arise in the management of critically ill obese patients, along with the unique physiology resulting from obesity.

RESPIRATORY MANAGEMENT

Obesity results in an alteration of the lung volumes and capacities, including a significant drop in functional residual capacity (FRC), vital capacity (VC), and tidal volume, while the residual volume (RV) and total lung capacity (TLC) are less affected.9 The expiratory reserve volume (ERV = FRC-RV) drops exponentially with increasing BMI, with the effect most pronounced in those with more central obesity. Even a BMI of 30 kg/m2 can reduce ERV by 53% compared to normal BMI. A 1% decrease in ERV can be expected for every additional unit of BMI.10 As a result of the lower tidal volumes and higher metabolic rate, the respiratory rate typically is higher.9,11

As might be expected, total respiratory compliance is lower by as much as two-thirds in obese patients, with contributions from fat deposition in the chest wall and abdomen, incomplete relaxation of respiratory muscles, and lower lung compliance. In fact, respiratory compliance appears to be inversely related to BMI,12 resulting from increased pulmonary blood volumes, closure of dependent airways, and increased alveolar surface tension at lower FRC.9 With rising BMI, the FRC can drop below the closing volume at which basilar alveoli start to collapse, resulting in ventilation perfusion (V/Q) mismatch and hypoxemia. The drop in FRC with anesthesia of normal BMI subjects is even more pronounced in patients with obesity.11 Similarly, obesity can dramatically decrease the time to desaturation in a pre-oxygenated patient who is apneic, such as during induction of anesthesia.11

Airway resistance also is increased in obese patients, in part because of the lower FRC.9 The lower respiratory compliance and higher airway resistance seen in these patients leads to an increase in the work of breathing. As a result, the oxygen cost of breathing at rest (the percentage of body oxygen consumption dedicated to respiratory muscle work) rises from a normal of less than 3% in nonobese subjects to a level that is four- to 10-fold higher in obese patients.9

Considering the respiratory physiologic changes in obesity noted above, methods to improve ventilation in these patients include reverse Trendelenburg position at 30-45 degrees,13,14 prophylactic bilevel positive airway pressure in the postoperative period,15 and higher levels of positive end-expiratory pressure (PEEP) up to 10 or even 15 cm H2O in those on mechanical ventilation.16,17 Recruitment maneuvers followed by PEEP 10 cm H2O during anesthesia and paralysis of obese patients likely is better than either alone in improving atelectasis, although the generalizability of all of these anesthesia studies to the ICU remains unclear.16,18,19 At present, while it is not unreasonable to trial a patient on higher PEEP followed by a reassessment of oxygenation, there are no strong data to indicate that all obese patients should be treated with higher PEEP. Similarly, there are insufficient data to suggest the routine use of recruitment maneuvers in obese patients.20

Short-term anesthesia studies on ventilator mode in obese patients have been conducted and suggest special considerations for the obese patient with ARDS. In a secondary analysis of the ARDSNet trial, O’Brien found no difference in outcome in acute lung injury when comparing normal, overweight, and obese subjects who were ventilated with 6 mL/kg predicted body weight (PBW), knowing that the study excluded patients with a weight (kg):height (cm) ratio 1.21 To achieve a tidal volume of 6 mL/kg PBW, one should aim for a plateau airway pressure of < 30. However, without data to support them, some would argue for the acceptance of a higher plateau pressure if needed, knowing that this does not necessarily translate into a high transpulmonary pressure, but rather reflects the lower chest wall compliance and higher abdominal pressure. When available, use of esophageal manometry can help to assess the contribution of the chest wall to total respiratory compliance.

An “obesity paradox” has been described when looking at mortality in ARDS and septic shock5,22 in that obese patients tend to have a better outcome compared to normal weight or underweight patients. However, further analysis has demonstrated that differences exist in the demographics (age, APACHE III score, types of infection) and treatment (intravenous [IV] fluid volumes used for resuscitation, antibiotic doses) of these groups and may better explain the differences in mortality. Further work needs to be done. It may be that we could improve the mortality of nonobese patients by studying some of these apparent paradoxes. Mogri et al provide a summary of practical tips for ventilating obese patients.23

OBSTRUCTIVE SLEEP APNEA AND OBESITY HYPOVENTILATION SYNDROME

The possibility of obstructive sleep apnea (OSA) or obesity hypoventilation syndrome (OHS) must be considered in obese patients, especially when managing the airway. Because many OSA patients remain undiagnosed,24 screening tools such as the STOP BANG questionnaire, which gives the patient a point for each of eight criteria (snoring, tiredness, observed apnea, pressure [hypertension], BMI, age, neck circumference, gender), are available. It was developed originally as a presurgical screening tool but has been expanded since for use in a broader population.25 The prevalence of moderate to severe sleep apnea in the general population is near 4% for women and 9% for men,26 and it increases to 48% for people with a BMI 30 kg/m2 in one study.27 The diagnosis of OSA puts patients at higher risk of acute hypercarbic and hypoxic respiratory failure, difficult intubation, pulmonary embolism, delirium, cardiac ischemia, arrhythmia, and other complications, especially in the postoperative period.24

Similarly, compared to those with OSA alone, those with OHS are at higher risk of complications such as respiratory failure, heart failure, prolonged intubation, hypertension, insulin resistance, pulmonary hypertension, postoperative ICU transfer, and longer ICU and hospital lengths of stay, especially in the postoperative period.28 A BMI > 30 kg/m2 and PaCO> 45 mmHg are critical elements of the diagnosis. While a diagnosis of OHS cannot be made when other etiologies of hypercarbia such as use of opiates and sedatives are present, precautions should be taken in these patients, including close respiratory monitoring and limiting the use of sedating medications when possible, especially since patients with untreated sleep-disordered breathing have an increased sensitivity to opiates. The prevalence is estimated to be 10-20% in obese patients with OSA and 0.15-0.3% in the general adult population.29 The risk of OHS goes up with BMI, and some estimate it at 50% in those with BMI  50 kg/m2. The combination of OSA, BMI > 30 kg/m2, and serum bicarbonate 28 mmol/L puts the patient at significantly higher risk of OHS, while a baseline serum bicarbonate 27 mmol/L makes a diagnosis of OHS much less likely (good negative predictive value).29

NUTRITION

Despite sufficient caloric intake, many obese patients remain malnourished, with a high rate of micronutrient deficiencies. In those who have undergone bariatric surgery, the American Society for Parenteral and Enteral Nutrition (ASPEN) recommends: initiation of thiamine prior to giving dextrose-containing IV fluids; evaluation for and treatment of micronutrient deficiencies, such as calcium, thiamine, vitamin B12, fat-soluble vitamins (A, D, E, K), and folate; and evaluation and treatment for deficiencies in the trace minerals iron, selenium, zinc, and copper.30

Obese patients with critical illness, similar to nonobese patients, are at risk for loss of muscle mass. Thus, hypocaloric, high-protein nutritional support often is recommended in these patients during times of critical illness, except in situations where high protein intake may be detrimental (progressive renal insufficiency, severe hepatic insufficiency, diabetic ketoacidosis, hypoglycemia, age > 60 years, or severe immune compromise).30 Indirect calorimetry, when available, is the best means of matching caloric replacement with expenditure. Short of this, the best equations for calculating caloric and protein needs in these patients are debated, making consultation with the nutritional support team critical.31

VENOUS THROMBOEMBOLISM

The risk of venous thromboembolism (VTE) is approximately 2.5 times higher in obese patients compared to nonobese patients, potentially due to altered levels of platelet activator inhibitor, plasma fibrinogen, factors VII and VIII, and von Willebrand factor; increased platelet activation; decreased mobility; venous stasis; and increased thrombin generation.32,33 Obese patients are more likely to have postoperative thromboembolism. Pulmonary embolism is the most common cause of postoperative mortality after bariatric surgery, accounting for approximately 50% of deaths in some studies.34,35

For deep venous thrombosis (DVT) prophylaxis with enoxaparin or dalteparin, standard doses (30 mg every 12 hours and 5,000 U once daily, respectively) are recommended up to BMI 40 kg/m2, with a 30% increase in dose for those 40 kg/m2. Even higher doses (enoxaparin 60 mg every 12 hours) are recommended by some for patients with BMI 50 kg/m2 who are undergoing bariatric surgery and are at high risk of DVT.36,37 Similarly, higher doses of unfractionated heparin for DVT prophylaxis are recommended by some experts.38

The diagnosis of VTE can be challenging in the obese patient, given the diminished quality of images seen as the result of higher BMI across all imaging modalities.33,35 Computed tomography (CT) remains the best modality for diagnosing PE. Lower extremity venous duplex exam remains the imaging modality of choice for DVT. Rather than using the typical linear ultrasound probe, a curvilinear ultrasound probe with 2-3 MHz frequency may result in better image quality.35

Treatment for DVT and pulmonary embolism (PE) in obese patients is similar to treatment in nonobese patients, with a few caveats. When using unfractionated heparin, using actual body weight rather than ideal body weight is recommended.39,40 Similarly, the American College of Chest Physicians (ACCP) Guidelines for anticoagulation suggest that weight-based (actual body weight) dosing for low molecular weight heparin (LMWH) is preferred over fixed dosing for obese patients; studies are limited in patients with weights > 144 kg (enoxaparin) and > 190 kg (dalteparin).41 For those with weights greater than these, no upper dose limit is recommended, but closer monitoring, potentially with Factor Xa levels, may be indicated.

Treatment recommendations for DVT and PE with the direct oral anticoagulants (DOACs) in those with BMI 40 kg/m2 or less are no different than in nonobese patients. However, DOACs generally are not recommended for use in patients with BMI 40 kg/m2 or weight > 120 kg because of the limited clinical data on safety and efficacy. If DOACs are used in those with BMI 40 kg/m2, it is suggested that drug-specific peak and trough levels (anti-Factor Xa, ecarin time, or dilute thrombin time, depending on the agent, or mass spectrometry drug levels) be monitored, limiting their use for many centers.42 As more data emerge on the safety and efficacy of these agents in patients with BMI > 40 kg/m2, the guidelines for use of DOACs in this population likely will evolve.43

PHARMACOLOGY

There is a paucity of research and information regarding drug dosing in this population, so consultation with the pharmacy service to assist with drug dosing and pharmacokinetics often is beneficial. Adjusted dosing of medications often requires the clinician to consider several theoretical considerations besides the usual renal and hepatic metabolism of the medication,44,45 including weight-based dosing. Weight-based dosing must consider whether the medication is best dosed on actual body weight (ABW) vs. ideal (IBW) vs. lean (LBW) vs. adjusted (ABWadj) body weight, knowing that one drug may require loading based on one weight criteria and maintenance dosing based on another weight criteria. Debate continues regarding the best size descriptor to use when calculating doses of renally cleared medications, and it is important to know which equations investigators used in the original dosing trials.46 Obesity may affect drug pharmacokinetics in several ways, including:

  • Absorption: increased oral absorption due to increased gastric emptying, decreased subcutaneous absorption, failure of intramuscular (IM) administration due to short needles.
  • Volume of distribution (Vd): increased Vd for lipophilic drugs. Thus, lipophilic medications often are loaded based on ABW while hydrophilic medications are dosed more often on LBW or IBW.
  • Metabolism through increased P450 2E1 activity and other effects.
  • Elimination: longer half-life of lipophilic drugs, increased glomerular filtration rate in obese patients with normal renal function, more difficulty calculating creatinine clearance in obesity and critical illness.

MANAGEMENT OF THE BARIATRIC SURGERY PATIENT

Because of the obesity epidemic, the number of patients undergoing bariatric surgery has grown, especially since it is one of the most effective treatments now available for the treatment of obesity and its complicating comorbidities. Because it is not uncommon for these patients to have complications requiring an ICU stay, a discussion of critical care in the obese patient would not be complete without some mention of bariatric surgery and its complications. As noted in the introduction, approximately 252,000 bariatric procedures were done in the United States and Canada in 2018.7 Of these, 61% were sleeve gastrectomy (SG), 17% were roux-en-Y gastric bypass (RYGB) procedures, 1% were gastric banding, 15% were revisions of prior surgeries, and the rest were much less commonly performed procedures. The mechanism of weight loss with SG is primarily restriction in the size of the stomach, while the RYGB not only results in restriction of gastric size, but also malabsorption, which needs to be considered when delivering enteral feedings in the ICU.

Mortality rates generally are < 1% after surgery, and < 10% of patients will require ICU admission. The most common complications leading to mortality and to ICU admission are PE, anastomotic leak, and cardiac events. The type of surgery affects the risk of complications and ICU admission, with fewer ICU admissions seen with laparoscopic compared to open procedures, and fewer seen with SG and gastric banding compared to RYGB.47 Additional factors associated with higher rates of ICU admission include age > 50 years, BMI 60 kg/m2, and the need for reoperation.

After PE, anastomotic leak is the second most common cause of preventable death after bariatric surgery. It occurs in up to 5% of patients, often leading to sepsis and carrying with it a mortality rate of 6-17%. Mortality rates are highest in those with a delay in diagnosis.47 Upper gastrointestinal contrast examination with water-soluble oral contrast is the investigation of choice to diagnose anastomotic leak in bariatric surgery patients.35,48 Small bowel obstruction, especially after RYGB and often from anastomotic stricture, internal hernia, and volvulus, is another relatively common postoperative complication that is best imaged by CT scan. Gastrointestinal bleeding is not uncommon, occurring in 1-2% of patients after RYGB, often at a staple line.

SUMMARY

Our healthcare system has made great strides in the care of many chronic diseases. Unfortunately, we continue to see a growing number of patients with obesity, the disease at the root of many of the chronic diseases facing our patients. As critical care practitioners, we will continue to see these patients in our ICU more frequently, requiring us to manage the unique medical problems and physiology seen in this population. Much of the data described earlier are based on anesthesia studies and studies of the otherwise healthy obese patient, while few studies have been done assessing the obese patient in the ICU. Thus, critical care of obese patients is an area ripe for further research as we face this challenge in the future.

REFERENCES

  1. [No authors listed]. Executive summary: Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: The evidence report. Obesity Research 1998;6(Suppl 2):51S-129S.
  2. Lemmens HJ, et al. Estimating ideal body weight — a new formula. Obes Surg 2005;15;1082-1083.
  3. Hales CM, et al. Trends in obesity and severe obesity prevalence in US youth and adults by sex and age, 2007-2008 to 2015-2016. JAMA 2018;319:1723-1725.
  4. National Heart, Lung and Blood Institute. Managing overweight and obesity in adults: Systematic evidence review from the Obesity Expert Panel, 2013. https://www.nhlbi.nih.gov/sites/default/files/media/docs/obesity-evidence-review.pdf.
  5. Ball L, et al. Obesity and survival in critically ill patients with acute respiratory distress syndrome: A paradox within a paradox. Crit Care 2017;21:114.
  6. Dennis DM, et al. Prevalence of obesity and the effect on length of mechanical ventilation and length of stay in intensive care patients: A single site observational study. Aust Crit Care 2017;30:145-150.
  7. American Society for Metabolic and Bariatric Surgery. Estimate of bariatric surgery numbers, 2011-2018. https://asmbs.org/resources/estimate-of-bariatric-surgery-numbers.
  8. Bercault N, et al. Obesity-related excess mortality rate in an adult intensive care unit: A risk-adjusted matched cohort study. Crit Care Med 2004;32:998-1003.
  9. Jaoude PA, et al. Effects of obesity on respiratory physiology. In: El Solh AA, ed. Critical Care Management of the Obese Patient, first ed. John Wiley & Sons, Ltd.; 2012:13-20.
  10. Jones RL, Nzekwu M-MU. The effects of body mass index on lung volumes. Chest 2006;130:827-833.
  11. Schumann R. Pulmonary physiology of the morbidly obese and the effects of anesthesia. Int Anesthesiol Clin 2013;51:41-51.
  12. Pelosi P, et al. The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg 1998;87:654-660.
  13. Burns SM, et al. Effect of body position on spontaneous respiratory rate and tidal volume in patients with obesity, abdominal distension and ascites. Am J Crit Care 1994;3:102-106.
  14. Perilli V, et al. The effects of the reverse Trendelenburg position on respiratory mechanics and blood gases in morbidly obese patients during bariatric surgery. Anesth Analg 2000;91:1520-1525.
  15. Joris JL, et al. Effect of bi-level positive airway pressure (BiPAP) nasal ventilation on the postoperative pulmonary restrictive syndrome in obese patients undergoing gastroplasty. Chest 1997;111:665-670.
  16. Pelosi P, et al. Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. Anesthesiology 1999;91:1221-1231.
  17. Erlandsson K, et al. Positive end-expiratory pressure optimization using electric impedance tomography in morbidly obese patients during laparoscopic gastric bypass surgery. Acta Anaesthesiol Scand 2006;50:833-839.
  18. Reinius H, et al. Prevention of atelectasis in morbidly obese patients during general anesthesia and paralysis: A computerized tomography study. Anesthsiology 2009;111:979-987.
  19. Almarakbi WA, et al. Effects of four intraoperative ventilatory strategies on respiratory compliance and gas exchange during laparoscopic gastric banding in obese patients. Br J Anaesth 2009;102:862-868.
  20. Fan E, et al. An official American Thoracic Society/European Society of Intensive Care Medicine/Society of Critical Care Medicine clinical practice guideline: Mechanical ventilation in adult patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2017;195:1253-1263.
  21. O’Brien JM Jr, et al. Excess body weight is not independently associated with outcome in mechanically ventilated patients with acute lung injury. Ann Intern Med 2004;140:338-345.
  22. Arabi YM, et al. Clnical characteristics, sepsis interventions and outcomes in the obese patients with septic shock: An international multicenter cohort study. Crit Care 2013;17:R72.
  23. Mogri M, Mador MJ. Mechanical ventilation of the obese patient, In: El Solh AA, ed. Critical Care Management of the Obese Patient, First Edition. John Wiley & Sons, Ltd., UK; 2012.
  24. Chan MTV, et al. Association of unrecognized obstructive sleep apnea with postoperative cardiovascular events in patients undergoing major noncardiac surgery. JAMA 2019;321:1788-1798.
  25. Chung F, et al. STOP-bang questionnaire: A practical approach to screen for obstructive sleep apnea. Chest 2016;149:631-638.
  26. Young T. Rationale, design and findings from the Wisconsin sleep cohort study: Toward understanding the total societal burden of sleep disordered breathing. Sleep Med Clin 2009;4:37-46.
  27. Chung F, et al. Predictive performance of the STOP-Bang score for identifying obstructive sleep apnea is obese patients. Obes Surg 2013;12:2050-2057.
  28. Kaw R, et al. Postoperative complications in patients with unrecognized obesity hypoventilation syndrome undergoing elective noncardiac surgery. Chest 2016;149:84.
  29. Chau EH, et al. Obesity hypoventilation syndrome: A review of epidemiology, pathophysiology, and perioperative considerations. Anesthesiology 2012;117:188-205.
  30. Taylor BE, et al. Guidelines for the Provision and Assessment of Nutrition Support Therapy in the Adult Critically Ill Patient, Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). Crit Care Med 2016;44:390-438.
  31. Bal BS, et al. Nutritional requirements of the critically ill obese patient. In: El Solh AA, ed. Critical Care Management of the Obese Patient, First Edition. John Wiley & Sons, Ltd., UK; 2012:186-196.
  32. Stein PD, et al. Obesity as a risk factor in venous thromboembolism. Am J Med 2005;118:978-980.
  33. Trow TK, Matthay RA. Management of venous thromboembolism in the critically ill obese patient. In: El Solh AA, ed. Critical Care Management of the Obese Patient, First Edition. John Wiley & Sons, Ltd., UK; 2012:108-115.
  34. Joffe A, Wood K. Obesity in critical care. Curr Opin Anaesthesiol 2007;20:113-118.
  35. Katabathina VS, et al. Diagnostic imaging of the critically ill obese patient. In: El Solh AA, ed. Critical Care Management of the Obese Patient, First Edition. John Wiley & Sons, Ltd., UK; 2012:135-148.
  36. Scholten DJ, et al. A comparison of two different prophylactic dose regimens of low molecular weight heparin in bariatric surgery. Obes Surg 2002;12:19-24.
  37. Borkgren-Okonek MJ, et al. Enoxaparin thromboprophylaxis in gastric bypass patients: Extended duration, dose stratification, and antifactor Xa activity. Surg Obes Relat Dis 2008;4:625-631.
  38. Shepherd MF, et al. Heparin thromboprophylaxis in gastric bypass surgery. Obes Surg 2003;13:249-253.
  39. Rondina MT, et al. The treatment of venous thromboembolism in special populations. Thromb Res 2007;119:391-402.
  40. Yee WP, Norton LL. Optimal weight base for weight-based heparin dosing protocol. Am J Health Syst Pharm 1998;55:159-162.
  41. Garcia DA, et al. Parenteral anticoagulants: Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest 1012;141:e24S-e43S.
  42. Martin K, et al. Use of the direct oral anticoagulants in obese patients: Guidance from the SSC of the ISTH. J Thrombo Haemost 2016;14:1308-1313.
  43. Kido K, Ngorsuraches S. Comparing the efficacy and safety of direct oral anticoagulants with warfarin in the morbidly obese population with atrial fibrillation. Ann Pharmacother 2019;53:165-170.
  44. Shashaty MGS, Stapleton RD. Physiological and management implications of obesity in critical illness. Annals ATS 2014;11:1286-1297.
  45. Erstad BL. Drug dosing in the critically ill obese patient. In: El Solh AA, ed. Critical Care Management of the Obese Patient, First Edition. John Wiley & Sons, Ltd., UK; 2012.
  46. MacDonald JJ, et al. The weight debate. J Intensive Care Soc 2015;16:234-238.
  47. Mimms SE, Mattar SG. Critical Care Management of the obese patient after bariatric surgery. In: El Solh AA, ed. Critical Care Management of the Obese Patient, First Edition. John Wiley & Sons, Ltd., UK; 2012:179-185.
  48. Chandler RC, et al. Imaging in bariatric surgery: A guide to post-surgical anatomy and common complications. AJR Am J Roentgenol 2008;190:122-135.