The “obesity paradox,” as it is termed, may at first glance seem counterintuitive, but on reflection by the experienced intensive care unit (ICU) clinician, it quickly is found to be consistent with clinical observation. The obesity paradox refers to a literature body that supports decreased mortality in obese ICU patients when compared to nonobese patients of otherwise-matched demography and complexity of illness. While the morbidly obese patient may need more complex care and may be more apt to suffer certain complications, the obese patient has also been shown to be more likely to survive. More simply, it has been shown that despite the increased morbidity associated with obese ICU patients, there is also an association of decreased mortality.

It is the goal of this chapter to highlight these potential areas of increased morbidity as well as areas where usual management schema will need to be adjusted to these patients’ unique physiology. Wherever possible, I draw attention to any available data specific to the obese female population, although the overwhelming bulk of available literature on this topic is not gender specific (Figure 13-1).

Infections and Antimicrobials

Obesity has been recognized as a risk factor for both morbidity and mortality in patients infected with H1N1 influenza. The Centers for Disease Control and Prevention (CDC) considers morbid obesity a high-risk condition for 2009 H1N1-related hospitalization and possibly death.¹ A study of 534 patients in California with H1N1 in 2009 found that, at a body mass index (BMI) of 40, the odds ratio (OR) of death was 2.8; for those patients with BMI greater than 45, the OR for death increased a further 50% to 4.2.¹ During the same year, a study of 1520 patients in the United Kingdom also identified obesity as an independent risk factor for H1N1-associated morbidity greater than that associated with delayed admission, pneumonia, and the need for supplemental oxygen.² There is also evidence that vaccination may be less effective in obese patients, with the rate of titer decay having been shown to be significantly more rapid in this population.³

Bacterial pneumonia as both a primary and a secondary infection has inconsistently been associated with obesity, but even in the studies that favored obesity as a risk factor for pneumonia, the paradox of increased survival generally remained present.^4,5,6 The development of community-acquired Clostridium difficile infection was associated with obesity in a 2013 Boston study.⁷ A 2008 randomized controlled trial found a higher rate of infection associated with femoral catheters placed in obese as compared to nonobese patients, while a 2009 study of over 2000 ICU patients found severe obesity to be a risk factor for catheter-related (OR 2.2) and other bloodstream infections (OR 3.2).^8,9 It is not known whether the biology of obesity is responsible for the aforementioned associations or if habitus itself is the progenitor of these complications.

I have long used whole-body chlorhexidine bathing for the morbidly obese population in the ICU. Anecdotally, we have had great success with this strategy, with the underlying assumption that increased skin surface and areas of intertrigo predispose to colonization and substantial bioburdens. In more recent years, there is evidence to suggest this practice be adopted to prevent central line–associated blood stream infections (CLABSIs) for all patients.^10,11 If the strategy is, in fact, effective, then one could postulate that patients with greater body surface area (BSA) should stand to enjoy the benefit from the intervention.

We know that obesity can, itself, predispose to infection.^12,13,14 We also know that the treatment of infection may be complicated by morbid obesity when one endeavors to adequately dose antibiotics, especially in the setting of life-threatening infection. Antimicrobials are often dosed by ideal or actual body weight, but this becomes problematic when the distribution volume of some antibiotics will so vastly exceed that predicted by any body weight dosing schema. This runs the risk of clinically important underdosing of antibiotics not only affecting the index patient but also contributing to resistance through pathogen exposure to subtherapeutic inhibitory concentrations.

There are data for piperacillin-tazobactam in patients with BMIs over 40 (study group mean BMI of 57) that showed that the dosing regimen of 4.5 g every 6 hours was adequate for minimum inhibitory concentration (MIC) attainment for likely pathogens in this population.¹⁵ Interestingly, the study found that the half-life of the drug was approximately 3-fold historical controls of normal BMI, which actually increased the area under the curve for time above MIC. This decreased clearance coupled with dosing at the highest end of the recommended range resulted in adequate dosing of piperacillin-tazobactam and is a theme seen with β-lactams in general.¹⁵

In a study of 48 critically ill patients on vancomycin, it was found that standard pharmacokinetic modeling was more likely to be inaccurate in obese patients.¹⁶ A 2014 literature review found that obesity was a significant confounder for accuracy of aminoglycoside dosing but, most troublingly, also found that the inaccuracy resulted in both subtherapeutic and supratherapeutic dosing.¹⁷ A study of carbapenem dosing was published in 2013 that concluded that the use of extended infusions could minimize the effects of patient weight and large volumes of distribution on achievement of adequate MICs.¹⁸ There are also data to implicate that almost 3-fold dosing can be required for lipophilic antibiotics (fluoroquinolones, macrolides, glycylcyclines, and lincosamides) in the obese population due to the enhanced adipose volume of distribution.^19,20 In obese patients on continuous renal replacement therapy, there are recommendations to dose ciprofloxacin as high as 800 mg every 12 hours.²¹

While there is a paucity of literature, overall general guidelines to aid the practitioner should be based on the pharmacokinetic data referenced above. Of note, a 2010 study found no correlation between increasing body weight and in vivo volume of distribution for the metabolite of oseltamivir with the plasma concentration exceeding the needed threshold many fold throughout the dosing interval.²²

Renal Failure

Renal failure has been observed to occur disproportionately in the obese critically ill patient. A study of 751 patients with acute respiratory distress syndrome (ARDS) found that the OR of acute kidney injury (AKI) increased by 1.2 for every 5 kg/m² increase in BMI. The same study also found that the OR for mortality was 0.81 for every 5 kg/m² increase in BMI.²³ Among 562 critically ill Canadian patients with H1N1, the OR for obesity as an independent predictor of AKI was 2.94, and the OR was 2.25 for renal replacement therapy.²⁴ Among 400 trauma patients, obesity was found to confer an OR of 4.72 for AKI.²⁵ The apparent propensity for renal failure in the obese patient may be biology, or it may be related to a tendency to underresuscitate in this population due to barriers in perception of what defines an adequate volume of crystalloid in an obese patient.

Hemodynamic Support

The first and most important reality to digest is that the volume of fluid that will be required to adequately resuscitate a morbidly obese patient may be in the tens of liters. The Surviving Sepsis Campaign recommends 30 kg/m² of initial bolus resuscitation to adequately challenge a patient in septic shock.²⁶ Some quick math yields some extraordinary numbers. These volumes, while they may seem extreme, are appropriate and suited to the extreme sizes to which they are ascribed. To use less in the face of ongoing hypoperfusion in respect of arbitrary norms of resuscitation would be inappropriate and an injustice to these patients. It should also be understood that the prevalence of obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS) in the population of patients with BMIs exceeding 40 is as high as 70% and 30%, respectively, in some studies.^27,28,29

This becomes important in a discussion of hemodynamic support when one realizes the prevalence of pulmonary hypertension and subsequent right heart failure this will engender. In practice, I assume embarrassed right heart function in the presence of morbid obesity and venous stasis of the lower extremities until echocardiography refutes that assessment. The presence of right heart dysfunction will generally magnify the usual fluid requirements in resuscitation of a vasodilatory shock.

The use of bedside ultrasonography often yields a technically limited evaluation in these patients due to their habitus further complicating their management by confounding, while not completely incapacitating, this tool that has become so common in the practice of critical care. If a pulmonary artery catheter is in place, some guidance can be gleaned from a 2006 study of 700 consecutive patients taken for angiography who had clean coronaries and a cardiac output (CO) measurement during the angiography. BMI was found to positively correlate with CO and stroke volume (SV). Each 1 kg/m² increase in BMI was found to give a 0.08 L/min increase in CO and 1.35 mL increase in SV.³⁰

Given the increased risk for AKI in this population, hemodynamic support and adequacy of resuscitation volume should be followed vigilantly by whatever means one chooses. There are no conclusive data to support one over another.

On the note of measurement, I would challenge the dogma of the superiority of invasive monitoring. There are no high-quality data in the literature to support improved outcomes with invasive versus noninvasive approaches of monitoring in critical care.^31,32 That said, upper arm girth may be a practical limitation to reliable blood pressure measurement; certainly, in absence of any other means to measure blood pressure, an arterial line will give you not only a reading but also a gold standard reading. Alternatively, there are relatively new products available designed to take forearm blood pressure measurements. At least one of these devices is clinically validated specifically for measuring blood pressure in the forearm of obese patients. (Critikon Radial-Cuf by GE Healthcare). Beyond these pitfalls, the principles of hemodynamic monitoring and resuscitation remain the same.

The primary pitfalls in the respiratory management of the obese patient relate to the weight of the chest wall, especially while supine, and its effect on the airway as well as mechanics of respiration. Obese patients are more prone to hypoxia than leaner individuals as a result of reductions in multiple pulmonary function parameters. They include forced vital capacity (FVC), forced expiratory volume in 1 second (FEV₁), expiratory reserve volume (ERV), functional residual capacity (FRC), and maximum voluntary ventilation (MVV).³³ Pregnancy also results in substantial reductions in ERV and FRC.³⁴ It is not known whether the usual increase in tidal volume of 30%–40% in pregnancy is attenuated in the obese patient by lower baseline ERV and FRC. Pulmonary complications of obesity include OSA and OHS and some have suggested asthma, although others have argued it is more a subjective dyspnea than true reactive airway disease.^35,36,37 This chapter also addresses the life-threatening pulmonary complications specific to pregnancy and where their diagnosis and management may be complicated by obesity.

Noninvasive Ventilation

The prevalence of OSA and OHS in this population is substantial, as mentioned previously, and should be anticipated when caring for the obese patient irrespective of initial indications for admission. This can include interventions such as screening with simple questions all the way to subspecialist consultation. Obese patients who are expected to receive sedatives or analgesics during their stay are at especially high risk for respiratory complications as any tendency for hypoventilation will be magnified by these drugs. These patients should be considered for more careful monitoring through means such as remote oximetry and capnography as well as tighter nursing ratios.

I recommend, in those patients for whom a surgical procedure is elective who screen positive for the possibility of OSA, that there be consideration given for deferment of elective surgery. Where surgery should not be deferred, patients should be considered for empiric monitoring and subspecialist consultation for the provision of empiric noninvasive positive pressure ventilation (NIPPV) in the postoperative setting. Certainly, for those patients who already carry the diagnosis of OSA or OHS, any outpatient management strategies already instituted should be carried over meticulously to the inpatient setting. In the patient who reports noncompliance with their prescribed continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) at home, it will be important to ensure compliance while hospitalized as their native dependence will only be magnified by the indications for and process of hospitalization. Further, I advocate for the aggressive use of NIPPV in this population for both chronic and acute indications.

The complexity of invasive airway instrumentation and invasive ventilation in these patients increases the potential for associated complications.^38,39,40,41 Therefore, if presented with an acute clinical scenario that is judged likely to improve in the coming hours to the point that the need for positive-pressure ventilation is expected to wane, it is reasonable to consider NIPPV for sedate patients who are judged to adequately protect their airway. These patients must be managed in an ICU setting where the ongoing level of sedation and response to therapy can be vigilantly monitored. Avoiding an intubation or reintubation in this population is of great benefit to the patient if it can be done safely.