Critical Care of the Morbidly obese Patient Louis Brusco Jr, MD, FCCM

Critical Care of the Morbidly
Obese Patient
Louis Brusco Jr, MD, FCCM
■ Recognize the comorbid conditions that affect the
critically ill, morbidly obese patient
■ Discuss the special pulmonary challenges in caring for
morbidly obese patients in the ICU
■ Explain the influence of the inflammatory cascade on
critical illness in the morbidly obese patient
■ Summarize the unique aspects of the nutritional man-
agement of the critically ill morbidly obese patient
■ Demonstrate the approach to drug dosing in the
morbidly obese patient in the ICU
■ Describe the extraordinary nursing care concerns of
the critically ill patient who is morbidly obese in the
Key words: morbidly obese patient; obstructive sleep
apnea; obesity hypotension syndrome
For thousands of years obesity was rarely seen.1 It was not
until the 20th century that obesity became common, so
much so that in 1997 the World Health Organization
(WHO) formally recognized obesity as a global epidemic.2
As of 2005 the WHO had estimated that at least 400
million adults (9.8%) were obese, with higher rates among
women than men.3 The rate of obesity also increases with
age, at least up to 50 or 60 years of age.4 Once considered a
problem only of high-income countries, obesity is increasing
worldwide. These increases have been felt most dramatically
in urban settings. The only remaining region of the world
where obesity is not common is sub-Saharan Africa.5
The United States has some of the highest obesity rates in
the developed world.6 From 1980 to 2002, obesity rates
doubled, reaching the rate of 32% of the adult population.7
Rates of obesity vary by ethnicity and gender. In the United
States, as of 2007, 33% of men and 35% of women were
obese.8 The rates, however, were as high as 50% among
African American women in 2005.9 The prevalence of class
III obesity (body mass index ≥40) has increased the most
dramatically, from 0.78% in 1990 to 2.2% in 2000.10
Although the overall rate of obesity began to plateau in the
2000s, severe obesity and obesity in children continue to
Obesity is one of the leading health issues in US society,
resulting in about 300,000 deaths per year in the United
States.11 About 65% of Americans are now considered either
overweight or obese.12 According to data from National
Health and Nutrition Examination Study collected from the
1970s to 2004, the prevalence of overweight and obesity has
increased steadily among all groups of Americans over the
past 3 decades.7 Obesity in other countries presents different
problems. Although the rates of obesity in Japan and Korea
are far less than in the United States, comorbid conditions
occur at lower weights so that obesity is a significant
problem in these countries as well.13
Nearly one-third of patients in ICUs meet the criteria for
obesity, and up to 7% are morbidly obese.14 Although it
may seem apparent that patients with obesity and morbid
obesity have higher morbidity and mortality rates when
critically ill compared with nonobese patients, and individual studies have indicated as much,15 this has not been
borne out in all studies and meta-analyses, including the
most recent one. Nevertheless, patients with morbid obesity
present management challenges when they are in the critical
care setting, from both the comorbidities that accompany
their illness and the differences in management that they
require. In the current obesity epidemic, every practitioner
of critical care medicine needs to be aware of these challenges and the management strategies that accompany them.
Comorbid Conditions
Workers with morbid obesity have high incidences of type 2
diabetes mellitus (10% in men, 20% in women), coronary
artery disease (14% men, 19% women), and hypertension
(64%).16 The prevalence of these conditions in patients who
are not able to work, who are more likely in a typical ICU
population, is at least this and probably higher. Clinicians
taking care of morbidly obese patients must be prepared for
exacerbations of preexisting comorbid conditions as well as
emergence of previously undiagnosed conditions that crop
up in the course of a critical illness.
Diabetes Mellitus
Diabetes mellitus is the most critical of all the comorbid
conditions, because diabetes places the patient at risk for
all of its own comorbidities. The link on a cellular level has
only recently been elucidated. Fat cells release a novel protein called pigment epithelium-derived factor, which triggers
a chain of events and interactions that lead to development
of type 2 diabetes.17 When pigment epithelium-derived
factor is released into the bloodstream, it causes the muscle
and liver to become desensitized to insulin. The pancreas
then produces more insulin to counteract these negative
effects. This insulin release causes the pancreas to become
overworked, eventually slowing or stopping insulin release
from the pancreas, leading to type 2 diabetes. Diabetes is
Current Concepts in Adult Critical Care
also involved, as seen later in this chapter, in the inflammatory changes accompanying morbid obesity.
Patients who are morbidly obese with preexisting diabetes
mellitus are at risk for all the comorbidities of diabetes and
disease states that accompany diabetes, such as diabetic
nephropathy, poor wound healing, diabetic gastroparesis,
and cardiac disease. Many patients with morbid obesity
will present with an existing diagnosis of diabetes and will
be at risk for the comorbidities; some patients will present
without such a diagnosis, but the critical illness will unmask
the disease process and the patient will show hyperglycemia
during the ICU course. These patients, despite their new
diagnosis of diabetes, can show remarkable resistance to
exogenous insulin, requiring surprisingly high doses of
insulin infusions: doses as high as 25 U/h are not unheard of.
Cardiac Disorders
Patients with morbid obesity can show a number of cardiac
disorders that make management in the ICU more difficult.
These patients have the previously mentioned increased
incidence of coronary artery disease and hypertension.
Patients with morbid obesity are frequently deconditioned
from a cardiac standpoint and frequently have a resting
tachycardia that can worsen during the course of critical
illness. Patients who are morbidly obese and have obstructive sleep apnea (OSA) have an increased incidence of cor
pulmonale and pulmonary hypertension that may make
monitoring of central venous pressures less reliable, but
rarely will OSA interfere with other management unless it
is a known diagnosis prior to the illness. Finally, between
tendencies toward diabetic nephropathy and hypertensive
renal disease, patients with morbid obesity can show very
little renal reserve and can show decreases in renal function
following surprisingly little in the way of a renal insult.
Pulmonary Concerns
The body system that most frequently is affected by obesity
is the pulmonary system. Such effects may be in the form of
increased incidence of conditions such as asthma or OSA,
difficulties managing the airway of a patient in pulmonary
failure, or difficulties with ventilation and weaning a
patient who is morbidly obese. The clinician caring for the
morbidly obese must be aware of these pulmonary aspects,
because they so frequently alter management.
Pulmonary Mechanics and Mechanical Ventilation
Patients with morbid obesity frequently have abnormal
mechanical properties of the total respiratory system, with
decreased compliance of both the lungs and the chest wall.18
This is likely due to increased blood pulmonary blood
volume; increasing lung compliance caused by closure of
dependent airways, and a small (if any) contribution from
the simple mechanical effect of adipose tissue pressing on
the thorax and increasing the effort needed to initiate a
breath. Airway resistance is elevated because of reduced
lung volumes, with a preserved ratio of forced expiratory
volume in the first second of expiration (FEV1) and forced
vital capacity indicating that the resistance is present in the
small airways and lung tissue rather than the large airways.
Obese patients without obesity hypoventilation syndrome
(OHS) have normal respiratory muscle strength, whereas
patients with OHS are approximately 30% weaker, thought
secondary to an overstretched diaphragm and possibly to
fatty infiltration of the diaphragm in some cases. Spirometry
frequently shows a decreased expiratory reserve volume
and an increase in the FEV1 to forced vital capacity ratio,
with preserved vital capacity, functional residual capacity,
total lung capacity, and maximum minute ventilation. The
decreased expiratory reserve volume in the setting of a normal vital capacity indicates an increased inspiratory capacity.
Patients with OHS will show more severe derangements of
pulmonary abnormalities, with decreased total lung capacity,
functional residual capacity, FEV1, and maximum minute
ventilation. Diffusion capacity is preserved in both sets of
patients, and oxygenation is only mildly impaired and then
mostly secondary to hypercapnea in patients with OHS.
There is no consensus on how to choose the settings for
mechanical ventilation of the morbidly obese patient, other
than it is incorrect to calculate tidal volumes based on
actual body weight (ABW). Patients with morbid obesity
have normal-appearing chest cavities on chest radiograph,
and such radiographs clearly show that these patients have
smaller lungs than would be expected based on their weight.
A common suggestion is to start with a tidal volume based
on ideal body weight (IBW) and then to adjust the settings
based on blood gas analysis. Starting with higher levels of
positive end-expiratory pressure to overcome basal atelectasis
is usually extremely helpful.
The effects of morbid obesity on pure pulmonary outcome
may be significant; one study showed that morbidly
obese patients with similar Acute Physiology and Chronic
Health Evaluation II scores had higher rates of nosocomial
pneumonias, acute respiratory distress syndrome, and
tracheostomy and a longer median length of mechanical
ventilation.19 The combination of increased abdominal
pressure, high volumes and low pH of gastric contents, high
incidence of diabetes mellitus, and resultant gastroparesis
puts these patients at higher than usual risk of aspiration of
gastric contents. Positioning and prophylaxis against acid
secretion, even in the absence of a history of gastroesophageal reflux disease, may be helpful, and prophylaxis against
deep venous thrombosis is even more important than in
nonobese patients.
At first glance, the airway of the morbidly obese patient
will usually appear more difficult to intubate than that of
a nonobese person. This is primarily due to the clinician’s
impaired ability to view the pharynx through the patient’s
open mouth, a measurement technique called the Mallempati classification. In nonobese patients, the degree to which
you can see the posterior oropharynx and tonsillar pillars is
Critical Care of the Morbidly Obese PatienT
one accurate predictor of difficulty of intubation; in obese
patients, the tongue tends to ride high and obscure the rear
of the mouth but still not get in the way of intubating the
patient. Far more important is the degree to which a patient
can extend his or her neck. This is limited, to a large degree,
by neck circumference, but it also has to do with the length
of the neck and whether the patient has posterior cervical fat
pads that will get in the way of extension of the neck when
lying supine. Many times, the difference between being able
to intubate or not is determined solely by the positioning.
The placement of bolsters under the shoulder blades, moving the posterior cervical fat pad off the table and allowing
the neck to extend, is often necessary to establish a secure
airway. Intubation of morbidly obese patients is also made
more difficult because the patients have limited physical
reserve and a lower functional residual capacity when supine
and thus desaturate quicker than nonobese patients, giving
the obese patient less time for intubation than a nonobese
Obstructive Sleep Apnea
From the first descriptions of the Pickwickian syndrome by
Burwell in 1956, it has been recognized that morbidly obese
patients have problems with apnea-related syndromes. The
Pickwickian syndrome is perhaps the most severe of these:
this syndrome describes patients who are morbidly obese;
have daytime hypersomnolence, dyspnea, plethora (from
polycythemia), and cyanosis (from hypoxemia); have both
hypoxemia and hypercapnea on arterial blood gases; and
have signs of pulmonary hypertension and right ventricular
failure. This all stems from the increased prevalence of OSA
in patients with morbid obesity. A full discussion of OSA is
beyond the scope of this text; an excellent review of OSA as
it relates to obesity was provided by Koenig in 2001.18 Older
estimates placed the incidence of OSA in patients with
morbid obesity at 42% to 48% in men and 8% to 38% in
women20; these figures may severely underestimate prevalence, given that newer studies show an incidence of 60% in
obese patients21 and nearly 70% in patients presenting for
bariatric surgery.22
Patients with OSA can present with chronic hypoxemia or
periodic desaturations leading to a chronic polycythemia,
chronic hypercapnia leading to pulmonary hypertension,
cor pulmonale and right ventricular failure, systemic
hypertension, and arrhythmias.
Management of the patient with OSA in the ICU will be
affected by the OSA in some manner. Given the use of
sedation and narcotics and changes in the patient’s mental
status, the clinician can expect earlier and more severe
worsening of respiratory status than otherwise expected.
Oxygenation levels may take months to improve and may
never “normalize,” so one may have to accept lower levels
of oxygenation when extubated. Weaning protocols based
on oxygenation and levels of CO2 must be interpreted in
light of the patient’s baseline. Mechanical ventilation of
the patient with OSA must avoid hyperventilation and the
resolution of the existing compensatory metabolic alkalosis.
Usual practice may include extubating to a noninvasive
ventilation standby with a higher frequency than would
occur with patients without OSA.
Asthma is reported in 30% of patients presenting for
bariatric surgery.23 Many patients with morbid obesity
have audible wheezing and many have been diagnosed
with asthma, but the wheezing may reflect an upper airway
condition and not true reactive airways disease. After
bariatric surgery, asthma symptoms are reportedly improved
in more than 75% of patients, leading one to doubt the
diagnosis. Although there may be some link between the
generalized inflammatory state as described subsequently
and the presence of reactive airways disease and asthma,
the clinician should not assume that these patients should
receive the usual treatment for asthma: some common
treatment decisions, like avoiding β-blockers or administering corticosteroids, may not be indicated.
The Role of Inflammation in Obesity
Recently interest has increased in the role of inflammation
in morbid obesity. C-reactive protein, an acute phase reactant, has undergone intense investigation,24 and it has been
found that the elevation of C-reactive protein corresponds
to the level of adiposity present in the body. Numerous
studies in obese subjects have shown high levels of tumor
necrosis factor-α and interleuken-6 (IL-6), the levels of
which decrease with weight loss and exercise. Insulin resistance is directly related to the degree of inflammation. The
adipose tissue mass seems to dictate the degree of inflammation in a linear fashion. There is progressive infiltration of
macrophages in adipose tissue that may be a major trigger
or sustainer of inflammation.25 In obesity and severe sepsis,
there is an increase in plasminogen activator inhibitor-1,
which can cause a marked decrease in fibrinolysis, and an
increase in tumor necrosis factor, which is either related to
or the actual cause of an exaggerated insulin resistance in
severe sepsis. Finally, there is an increased response of IL-6,
the clinical meaning of which is unknown but undoubtedly is somehow related to the exaggerated inflammatory
response that morbidly obese patients experience in severe
sepsis. This exaggerated inflammatory response relates to the
• Adipose macrophage infiltration
• Insulin resistance
• Exaggerated IL-6 response to additional inflammatory
• Increased leukocyte adhesion
• Increased platelet adhesion
• Increased pulmonary microvascular permeability
• High resting oxidative milieu
• Genomic differences between obese and lean tissue
The clinical implications of this are very critical. It is
clear that the inflammatory response in obese patients is
Current Concepts in Adult Critical Care
very different from that in nonobese patients. There are
anecdotal reports of increased response to drotrecogin alfa.
Patients with morbid obesity, besides having decreased
physical reserve from associated cardiac and pulmonary
conditions, can deteriorate rapidly and need quick and
decisive intervention. A “wait and see” approach is usually
not an option because these patients will deteriorate in a
vast storm of systemic inflammatory response syndrome that
is tough to recover from. All treatments of a severely septic
patient, such as antibiotic treatment, source control, and
hemodynamic support, need to be instituted swiftly. Even if
the patient has not been previously diagnosed with diabetes
mellitus, clinicians should provide adequate glucose control
and anticipate the need for high levels of insulin infusions.
Nutritional Aspects
Patients with morbid obesity in the ICU do not appear, at
first glance, to present difficulties with nutrition, and discussions about when to feed and how much to feed sometimes
can take on a demeaning tone among uncaring providers. In
comparison to nonobese patients, morbidly obese patients
in the ICU have the following characteristics:
• Higher glucose levels with more exaggerated response to
• Lower human growth hormone levels but normal response
to stress
• Higher insulin levels with lower response to stress
• Higher cortisol levels with normal response to stress
• Higher norepinephrine and epinephrine levels with much
lower response to stress
• Higher levels of ketones and free fatty acids.
• Normal resting energy expenditure with higher muscle
and nitrogen loss in ICU
This means that despite huge fat stores, patients with
morbid obesity can develop protein calorie malnutrition
very rapidly during critical illness. This is because the
increased baseline insulin levels suppress lipid mobilization
from fat stores and enhance protein breakdown to fuel
gluconeogenesis. The critically ill patient will degrade up to
50% more body protein than the nonobese patient, in part
because the inflammatory response increases the need for
paralyzing agents, sedation, prolonged bed rest from longer
times on the ventilator, and prolonged and higher amounts
of inotropic and pressor support and also because of the
generalized metabolic insult that these patients sustain. The
clinical consequences of protein catabolism are severe, and
steps need to be taken to combat this process.
Unfortunately, determining the proper amount of caloric
and protein replacement is not easy or well elucidated.
The best method to determine caloric needs is indirect
calorimetry, because using the Harris-Benedict equation is
inaccurate secondary to trouble deciding just what weight to
use, with an error rate of 74% using ABW and 36% using
adjusted body weight (AdjBW) with an increased incidence
of underestimation.26 In the absence of indirect calorimetry,
a current recommendation is to give 20 to 30 kcal/kg/d on
an obesity-adjusted weight as follows27:
IBW + (ABW – IBW) × 0.025
The main question for feeding morbidly obese patients in
the ICU is whether to use hypocaloric feedings, that is,
feedings that meet protein requirements but provide fewer
calories than expended. Some studies have shown a benefit
to hypocaloric feedings, in terms of decreased ICU stay,
fewer days of antibiotics, and a trend toward fewer days of
mechanical ventilation.28 Other studies are more equivocal,
so the issue is still debated. As with any type of critically
ill patient, the enteral route is preferable to the parenteral
Pharmacologic Concerns
Drug dosing provides daily challenges in the care of the
critically ill patient. Volumes of distribution may vary
widely depending on the patient’s amount of muscle mass,
adipose tissue, and edema, and 3 patients with the same
illness and same body weight may have widely differing
drug dosing requirements based purely on body composition. Ideally, a size descriptor would be available that would
take into account all the important measures: age, sex, race,
height, weight, edema status. Unfortunately, none of the
available descriptors take into account all of these factors
and none are terribly accurate in determining drug dosing
for all drugs on a consistent basis. Nonetheless, 2 have
become favorites in determining drug dosing, so they are
worthy of mention.
Ideal body weight (IBW) is a surrogate for lean body mass
and is possibly the most commonly used. Surprisingly, the
most common method of calculation, the Devine method,
comes from a reference in 1974 with unclear origins, has
not been since validated or updated, and is in article about
gentamicin dosing. This method is used in many pharmacokinetic studies of obesity and is calculated as follows29:
IBW (males) = 50 kg + 2.3 kg/in > 5 ft
IBW (females) = 45.5 kg + 2.3 kg/in > 5ft
Adjusted body weight (AdjBW) is usually used for dosing
patients with mild to moderate obesity, and it assumes
distribution of drug limited to some portion of excess
weight. It is often used if ABW is between 130% and 200%
of IBW. It is calculated as follows:
AdjBW = (ABW – IBW) 0.4 + IBW
Obesity causes functional changes in the body’s handling of
drug in a number of areas: blood flow changes, metabolic
changes, and binding changes. The changes may affect the
volume of distribution (Vd) of a drug or the clearance (Cl)
of a drug and may complicate an already confusing situation
in the ICU. The situation is further complicated when
Critical Care of the Morbidly Obese PatienT
clinicians try to determine the patient’s body composition—including muscle, adipose tissue, and edema—and
how it changes during the ICU stay, both of which affect
drug dosing.
Some generalizations are in order. Patients with an
ABW within 120% of IBW are unlikely to have clinical
consequences based on weight choice for drug dosing. Vd
tends to increase with more lipophilic medications, and,
somewhat vice versa, a small Vd (<15 L) reflects restriction
to extracellular space. Vd is most unpredictable for highly
lipophilic drugs with large Vd. There is no one good single
reference or chart to use for dosing. Some specific examples
Some of this discussion of vancomycin may apply to
β-lactam antibiotics. Vancomycin experiences a large
increase in Vd but an even larger increase in Cl.30 As with
β-lactams, there is non–concentration-dependent killing,
and side effects from overdosing are not nearly as severe as
with aminoglycosides. For severe infections, one does not
want to err on the low side of dosing, particularly when
there are penetration concerns, such as for pneumonia and
meningitis. Substantial variations occur in the morbidly
obese patient. The changes in Cl are more dramatic than the
change in Vd, so there is a shortened drug half-life, leading
to the suggestion that the dosing interval be decreased to
every 8 hours for vancomycin as well as the suggestion
that the drug be administered via continuous infusion.
Regardless, measuring of levels is paramount in this patient
Low-Molecular-Weight Heparin
Daily dosing of low-molecular-weight heparins is commonly suggested for reasons of cost and convenience. In
certain patient populations, however, such dosing may not
be sufficient. Trauma patients, even those who are not obese,
suffer low troughs with once-daily dosing of subcutaneous
enoxaparin.31 There are increases in drug Cl and Vd in
obesity that are not proportional to the increases in body
weight, and bleeding concerns arise if ABW is used to
calculate drug dosing. The suggestion has been made that
using AdjBW with more frequent dosing (ie, every 8 hours)
may be preferable to using ABW or IBW for calculating
enoxaparin dosing.32
Special Nursing Considerations
Patients with morbid obesity present special concerns
for nursing care. Patients are at staggering risk for the
development of pressure ulcers for a number of reasons. The
decreased perfusion of adipose tissue puts that tissue and the
overlying skin at risk for reduced blood flow. The weight of
the patient above the part of the body that is in contact with
the mattress combined with any local low-blood-flow states
makes these patients particularly susceptible to development
of pressure ulcers, which may show up days or weeks after
an episode of shock. Because of size and weight, patients
are difficult to turn and keep in a turned position and
have difficulty tolerating positions that are not supine. For
these reasons, patients who are expected to be in bed for
more than a few days should have a special bed or mattress,
preferably one that is optimized for bariatric patients and
has low air-loss surfaces with pressure relief features. Patients
who are in shock should be considered to be at especially
increased risk. Early recognition and treatment of pressure
ulcers, including surgical débridement are essential.
All areas of the skin, not just those that are under pressure,
are at high risk for breakdown and delayed wound healing,
especially in the skinfolds, where the moist conditions
harbor pathogens and induce breakdown of integumentary
barriers. To prevent this, daily inspection and frequent
scheduled turning are essential. The placement of powders
in skinfolds actually worsens skin breakdown and should be
avoided. Skin must be protected against pressure, shearing,
and pinching, and this is especially necessary when using
artificial lifts and springs to help turn the patient. Tubes
such as Foley catheters should not be placed in skinfolds, as
this will promote skin breakdown in those areas. If the ICU
has a large census of critically ill morbidly obese patients,
then procurement of specialized bariatric equipment,
such as movable sliding air mattresses, patient lifts, and
specialized bed chairs, may be warranted. Other special
equipment, such as blood pressure cuffs and laryngoscope
handles, is frequently needed.
Proper positioning is crucial for optimal pulmonary toilette.
The least beneficial positions are the supine, Trendelenburg,
lithotomy, and prone positions: these promote dyspnea,
atelectasis, and hypoxemia. Slightly better is the so-called
cardiac chair position, but in this position the pannus usually gets in the way of proper diaphragmatic excursion. The
most beneficial position is the lateral decubitus position, if
the patient will tolerate it, because it allows for displacement
of the abdomen and greater diaphragmatic excursion. The
30° to 45° semirecumbent position has similar properties
and is helpful in the immediate postoperative period.
Patients with morbid obesity present many challenges
to their care in the ICU, but with proper management
they can enjoy treatment success near to that of nonobese
Current Concepts in Adult Critical Care
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