Page 1839 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

1308 PART 11: Special Problems in Critical Care

occlusion pressure response to carbon dioxide is reduced in OHS obese (average BMI = 53 kg/m ) patients scheduled for gastric bypass
2
compared to normal individuals and to patients with simple obesity. surgery. Further, obesity is associated with a disproportionate rise in
31
Diaphragm electrical activity in response to carbon dioxide is inap- V O 2RESP for a given increase in minute ventilation, similar to emphysema.
32
propriately low in OHS. In obese patients with OSA, hypercapnea is Together these data suggest reduced respiratory reserve in extreme
associated with the severity of OSA, with increasing BMI, and with obesity, thereby increasing the risk of respiratory failure even from
the degree of restrictive chest wall mechanics. 22 seemingly trivial insults (eg, viral infection or, particularly in the post-
■ OTHER EFFECTS OF OBESITY operative patient, atelectasis) in a manner analogous to emphysema or
other chronically compensated forms of respiratory failure.
cantly with obesity, to as high as 40% when the BMI exceeds 40 kg/m . ■ EVALUATION OF RESPIRATORY FAILURE
Not surprisingly, the risk of obstructive sleep apnea increases signifi-
2
Increasing obesity probably promotes pharyngeal collapsibility not only The evaluation of extremely obese patients with critical illness and
through an increase in pharyngeal adiposity but also by decreasing respiratory failure, in particular, is challenging. Physical examination
radial traction on the upper airway through reductions in end expi- is difficult, and chest radiography is commonly unhelpful. Computed
ratory lung volume. 23,24 Obstructive sleep apnea may exacerbate and tomography and other similar diagnostic studies may be impossible if
promote cardiovascular disease through its hemodynamic effects on the the patient exceeds the weight limit or width of the scanner table. Even
heart as well as by increasing sympathetic outflow and oxidative stress. when such studies are possible, there are enormous technical and safety
25
Patients who successfully lose a significant amount of weight, usually challenges that accompany the transfer of such patients throughout the
via surgical approaches to weight reduction, may exhibit significant hospital. Frequently, diagnoses must by necessity be made on the basis
improvements in lung volumes, gas exchange, and work of breathing, of other clinical criteria.
and sleep-disordered breathing may improve or even resolve. The diagnosis of pulmonary edema is often frustrated by uncertainty
Intraabdominal pressure is elevated in obesity, placing the patient at regarding the presence of edema on the chest radiograph. Soft tissue
26
increased risk for the abdominal compartment syndrome, a potentially shadows on portable chest radiographs are often difficult to distinguish
lethal and under recognized complication of critical illness (see Chap. 114). from airspace edema. When suspected, other clinical signs may assist in
Indeed, BMI has been identified in a multicenter study as a risk factor for making a diagnosis. For example, abundant frothy secretions from the
the development of intraabdominal hypertension. A recent study also endotracheal tube commonly accompany pulmonary edema. Analysis
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demonstrated that many extremely obese (BMI 38-80.7 kg/m ) individuals of the protein content of the initial secretions may permit a distinction
2
have positive (elevated) pleural pressures throughout the chest at relax- between high- and low-pressure edema, as the latter is associated with a
ation volume, although the elevation was not predictable from BMI, waist protein content greater than one-half that of serum. Measurement of a
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circumference, or sagittal abdominal diameter. This finding suggests that frankly elevated B-type natriuretic peptide level supports the diagnosis
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respiratory and lung compliances are low in obesity as a result of breath- of pulmonary edema in the extremely obese patient with acute hypox-
ing at low lung volumes. It also highlights a limitation of static measure- emic respiratory failure. Similarly, pulmonary edema may be diagnosed
ments of cardiac filling pressure in assessing fluid responsiveness, given in the patient with hypoxemia refractory to high-flow oxygen who
that higher filling pressures would be required in such patients in order to also has an elevated right atrial pressure and abnormal left ventricular
achieve the same transmural pressure. systolic or diastolic function, although this approach also makes an
An intriguing association between obesity and chronic kidney disease inference that pulmonary edema necessarily results from abnormal
is becoming apparent. Certainly obesity is associated with diabetes pump function. Acute lung injury may be diagnosed on the basis of
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mellitus, hypertension, and cardiovascular disease, all of which predis- appropriate setting (eg, aspiration after the administration of sedatives)
pose to the development of chronic kidney disease. There is increasing and hypoxemia refractory to high-flow oxygen. Although differentiating
evidence, however, that obesity is an independent risk factor for chronic this condition from atelectasis can be difficult, noting abundant protein-
kidney disease. Obesity is associated with increased renal blood flow rich endotracheal secretions may be helpful.
and glomerular hyperfiltration that may subsequently lead to sclerosis. Pulmonary embolism is another serious condition that is particularly
Interestingly, obesity-related nephropathy may be mediated by the difficult to diagnose in the extremely obese patient. Computed tomog-
adipocyte itself. The adipocyte not only is an important component raphy of the chest and pulmonary angiography may be technically
of the renin-angiotensin-aldosterone system but also elaborates a variety unfeasible. Serial lower extremity Doppler examinations should be per-
of substances including leptin, free fatty acids, plasminogen activator formed, although pulmonary embolism is not disproved solely through
inhibitor-1, and proinflammatory cytokines, all of which may promote this approach. A normal D-dimer as determined by enzyme-linked
kidney injury. immunosorbent assay reliably excludes the diagnosis, but such a result is
The risk of venous thromboembolism is greatly increased in obese unlikely in the critically ill population, given the multitude of conditions
patients (BMI >30 kg/m ). Inactivity, venous stasis, and hypercoagu- associated with elevations in D-dimer levels. Echocardiography may
2
lability likely contribute to this risk. The risk of death from cancer is suggest the diagnosis by demonstrating acute right heart dysfunction,
lowest in individuals with a normal BMI and increases along with BMI. 9,30 but this finding lacks specificity given the range of disorders precipitating
respiratory failure (eg, acute lung injury, overlap syndrome, OHS, etc)
that cause this. Because there are no good data to guide the clinician,
MANAGEMENT OF RESPIRATORY FAILURE our approach is to initiate therapeutic anticoagulation in the setting of
■ PATHOPHYSIOLOGY OF RESPIRATORY FAILURE IN EXTREME OBESITY significant pulmonary hypertension (mean pulmonary artery pressure
>40 mm Hg), if acute right heart dilation without another satisfactory
Extremely obese patients may be particularly susceptible to respiratory cause is present, or when historical features (eg, acute onset of chest pain
failure. Under normal conditions, very little (<5%) of the body’s total and dyspnea) suggest the diagnosis.
Emphysema and other forms of chronic lung disease increase the oxygen ■ MANAGEMENT OF RESPIRATORY FAILURE
) is attributable to the work of breathing.
oxygen consumption (V O 2
) by increasing the load on Noninvasive positive pressure ventilation (NIV) may confer several
consumed by the respiratory muscles (V O 2RESP
the respiratory muscles. In such conditions, the strength of the respira- potential benefits in the initial management of extremely obese patients
tory system may be just adequate for the load on the system, and further with respiratory failure, including unloading the respiratory muscles,
insults, however trivial, may provoke respiratory failure. decreasing atelectasis, and treating any underlying sleep-disordered
Evidence suggests that extremely obese patients may be similarly breathing. It may also have a role in preventing respiratory complica-
averaged 16% in a group of extremely tions in the postoperative period, as discussed below. We recommend
compromised. Baseline V O 2RESP

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