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* From the Department of Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, James P. Nolan Clinical Research Center, University at Buffalo School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY.
Correspondence to: Ali El-Solh, MD, Division of Pulmonary, Critical Care, and Sleep Medicine, Erie County Medical Center, 462 Grider St, Buffalo, NY 14215; e-mail: solh{at}buffalo.edu
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Abstract |
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Design: A retrospective study.
Setting: Two university-affiliated hospitals.
Methods: We reviewed the medical records of 117 morbidly
obese patients (body mass index 
40 kg/m2) admitted to
the medical ICU between January 1994 and June 2000. Data collected
included demographic information, comorbid condition, APACHE (acute
physiology and chronic health evaluation) II score, invasive
procedures, organ failure, and in-hospital mortality.
Results: Obstructive airway disease, pneumonia, and sepsis were the main reasons for admission to the ICU in the morbidly obese group. Sixty-one percent of the morbidly obese patients and 46% of the nonobese group required mechanical ventilation (p = 0.02). The mean lengths of mechanical ventilation and ICU stay were significantly longer for the morbidly obese group (7.7 ± 9.6 days and 9.3 ± 10.5 days vs 4.6 ± 7.1 days and 5.8 ± 8.2 days, respectively; p < 0.001). APACHE II scores were not significantly different in the two groups (19.1 ± 7.6 and 20.6 ± 12.2; p = 0.6). Overall mortality was 30% for the morbidly obese patients and 17% for the nonobese group (p = 0.019). By multivariate analysis, multiorgan failure (odds ratio [OR], 4.6; 95% confidence interval [CI], 2.1 to 16.6), PaO2/fraction of inspired oxygen < 200 for > 48 h (OR, 2.3; 95% CI, 1.2 to 7.8), and depressed left ventricular ejection fraction < 40% (OR, 1.4; 95% CI, 1.03 to 13.8) were independently associated with ICU mortality in the morbidly obese group.
Conclusion: We conclude that critically ill morbidly obese patients are at increased risk of morbidity and mortality compared to the nonobese patients.
Key Words: APACHE II • central venous access • ICU • mortality • obesity • outcome • mortality
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Introduction |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Obesity has been linked to increased morbidity and mortality resulting from acute and chronic medical problems, including noninsulin diabetes mellitus, hypertension, dyslipidemia, cardiovascular disease, gallstones, cholecystitis, arthritis, and certain forms of cancer.1 It is speculated that morbid obesity increases the incidence of complications in patients requiring intensive care and that these complications are associated with prolonged hospital stay and poor outcome. However, very few data on critically ill obese patients have been collected, and ICU survival statistics are not available for this particular subset of the population. Two reviews7 8 acknowledged the lack of studies addressing the impact of obesity on ICU outcome. Hence, we conducted a retrospective study to test the hypothesis that morbidly obese critically ill patients are at an increased risk of morbidity and mortality, and to identify discriminant prognostic factors of survival using multivariate analysis.
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Materials and Methods |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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40
kg/m2. Patients were identified by
cross-referencing our demographic ICU database from January 1994 to
June 2000 with the International Classification of Diseases
codes listing all obesity categories. Computer-generated random
numbers were used to select the nonobese group sample (BMI < 30
kg/m2) in proportion to the number of morbidly
obese patients over the same time period. Patients who remained in the
ICU for < 24 h were not included in the study. The admissions
comprised of inpatient transfers and emergency department admissions.
For those patients with more than one ICU admission during the study
period, only the first ICU admission was included in the analysis to
ensure independence of observations.
Data Abstraction and Variable Definition
The data collected were of two categories: demographic and ICU
related. Demographic data included age, gender, height, weight, ICU
admitting diagnosis, smoking history, recent drug abuse, and comorbid
conditions (Table 1
).
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The development of organ failure was identified according to the following manner9 : liver failure, a serum bilirubin level > 6 mg/dL and a prolongation of the prothrombin time at least 4 s greater than the control; renal failure, a serum creatinine level > 3.4 mg/dL, the need for hemodialysis or peritoneal dialysis; respiratory failure, the need for intubation and mechanical ventilation; hematologic failure, a WBC count < 2.0/µL and/or platelet count < 40,000/µL; neurologic failure, a Glasgow coma scale score < 8 for > 24 h in the absence of sedatives, analgesics, or neuromuscular blockade; cardiovascular failure, the need for dobutamine or vasopressors (norepinephrine, or epinephrine at any dose, or dopamine at > 8 µg/kg/min); GI failure, documented GI bleed associated with a drop in hematocrit, pancreatitis, or bowel obstruction preventing enteral feeds for at least 48 h. Multiorgan failure (MOF) was defined as the presence of three or more organ failures.
Systemic inflammatory response syndrome (SIRS), sepsis, and septic shock were defined according to the American College of Chest Physicians and the Society of Critical Care Medicine Consensus Conference.10 ARDS was defined according to the American-European Consensus Conference.11 The causes of respiratory failure were classified into four subtypes. Type 1 is acute hypoxic respiratory failure referred to any alveolar-filling pathology present on chest radiography associated with impaired gas exchange (eg, pulmonary edema, ARDS, pneumonia). Type 2 is hypercapnic respiratory failure referred to any process associated with excessive respiratory load, impaired neuromuscular function, or a decreased ventilatory drive (eg, obstructive lung disease, obesity hypoventilation, muscle weakness). Type 3 is metabolic respiratory failure referred to any state of severely deranged acid-base disorder leading to the need of mechanical ventilation. Type 4 is airway protection-related respiratory failure. Type 4 respiratory failure was not considered evidence of organ dysfunction. If the cause of respiratory failure was multifactorial, the patient was classified by the primary reason for intubation and mechanical ventilation as discerned from the ICU progress notes. The immediate cause of death and code status with regard to "do not resuscitate" orders were noted.
Medical records were reviewed by two separate data extractors
experienced in critical-care chart abstraction. Information from charts
was logged onto a standardized computer data collection form.
Interobserver quality control was assessed by having an associate
coordinator re-enter 10% random sample of enrolled subjects. The
spreadsheet of the original and quality control was evaluated using the
statistic.12
All values 0.75 are considered
excellent agreement beyond chance; values < 0.4 are considered poor
agreement beyond chance; values between 0.4 and 0.75 represent
fair-to-good agreement beyond chance. The interobserver agreement for
this study was = 0.85 (95% confidence interval [CI], 0.64 to
0.97).
Statistical Analysis
Parametric interval data were analyzed using a two-tailed
Student’s t test. These data are reported as mean ± SD.
Nonparametric data were examined using a Mann-Whitney U test
or Kruskal-Wallis test as appropriate. Nominal data were analyzed by
2 analysis with Yates continuity correction or
Fisher’s Exact Test where appropriate. A multiple linear regression
was used to evaluate differences in length-of-stay variables (days on
the ventilator and in the hospital) after controlling for gender,
number of comorbidities, and APACHE II scores in obese and nonobese
patients. These covariates were selected because they may act as
confounders of the relation between severity of illness and length of
stay. Then, we conducted a forward stepwise logistic regression to
ascertain which factors contributed independently to mortality, with
hospital death as the dependent variable, and the retrospectively
identified independent variables including gender, APACHE II score,
BMI, and comorbidities. Another analysis was performed on the group of
117 patients using those variables found significant at p < 0.10 in
univariate analysis, with in-hospital mortality as the dependent
variable. Pairwise correlations between predictor variables and the
variance inflation factor were computed to assess for
multicollinearities according to the method described by Slinker and
Glantz.13
As for influential observations, no patients
with outlier values in any variable were detected. Mortality odds
ratios (ORs) were expressed with their 95% CIs. A p value < 0.05 was
considered significant. All statistical analyses were performed using
software (SPSS, version 10.0; SPSS; Chicago, IL).
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Results |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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60-year age group.
There were no age or gender differences between the two groups;
however, patients in the morbidly obese group had significantly higher
prevalence of cardiac, pulmonary, and endocrine comorbidities (Table 2)
. The presence of hypertension and sleep-related disorders were more
commonly reported in the morbidly obese group compared to the nonobese
group. Seventy-seven patients (66%) in the morbidly obese group were
being treated for hypertension, and 18 patients (15%) were prescribed
continuous positive airway pressure for documented obstructive sleep
apnea. In contrast, 39 of the patients in the nonobese group (29%) had
a history of elevated BP, while none had documented sleep-related
disorders (p < 0.001). Immunodeficiency was more frequently denoted
in the nonobese group: 11 patients (8%) vs 1 patient (1%)
[p < 0.014]. This observation is attributed mainly to the presence
of eight patients with AIDS in the nonobese cohort.
ICU Course
The reasons for ICU admission, the need for mechanical
ventilation, and the associated mortality for the morbidly obese and
the nonobese groups are provided in Table 3
. Pneumonia and reactive airway disease were the main reasons for ICU
admission in both groups. No predominant pathogen was responsible for
the cases of infectious pneumonitis, nor was there a
characteristic radiographic pattern that would characterize one group
from the other. Asthma was the predominant disorder of the reactive
airway disease in the morbidly obese group (10 of 14 patients; 71%),
whereas COPD was the prevalent disorder in the nonobese group (11 of 13
patients; 84%).
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In-hospital Mortality
The in-hospital mortality rate was 30% (35 of 117 patients) in
the morbidly obese group and 17% (22 of 132 patients) in the nonobese
group (p = 0.02). The immediate causes of death in the morbidly obese
group were bacterial infections in 17 patients; right ventricular
failure in 5 patients; acute pancreatitis in 4 patients; pulmonary
embolus in 2 patients; congestive heart failure in 3 patients; and
intracranial hemorrhage, liver failure, renal failure, Stevens-Johnson
syndrome each in 1 patient. A "do not resuscitate" order was
written for 9 patients (8%) in the morbidly obese group during the
course of their hospitalization, compared to 14 of the nonobese
patients (11%). None of the obese patients had prior advance
directives before the ICU admission.
The in-hospital mortality rate of morbidly obese patients requiring
mechanical ventilation was 49% (35 of 71 patients). Nineteen of the 40
obese patients (48%) who received mechanical ventilation for pulmonary
disorders died, compared to 16 of 31 patients (52%) in the same group
who required mechanical ventilation for nonpulmonary disorders
(p = 0.91). In contrast, the in-hospital mortality for morbidly obese
patients with documented depressed left ventricular ejection fraction
(LVEF) < 40% was 55% (12 of 22 patients), compared to 26% (17 of
65 patients) for those with LVEF 40% (p = 0.03). In the multiple
logistic regression, APACHE II score (OR, 1.11; 95% CI, 1.04 to 1.18),
cirrhosis (OR, 3.45; 95% CI, 1.69 to 5.82), and BMI (OR, 1.58; 95%
CI, 1.13 to 2.22) were all independent predictors of hospital death.
SIRS developed in 61 of the 117 morbidly obese patients (52%). The most common causes of SIRS were infection, which accounted for 45 of the 61 cases (74%), and acute pancreatitis, which was responsible for 9 of the 61 cases (15%). One or more organ failures occurred in 89 of the 117 hospital admissions (76%). The distribution of organ failures is presented in Table 4 . The median number of organ failures in those who survived was one, compared to three organ failures in those who died during hospitalization (Table 5 ).
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Fourteen of 117 morbidly obese patients (12%) underwent tracheostomy during the ICU stay, while only 5 of the nonobese patients (4%) had the same procedure (p = 0.03). Three of the 14 patients with morbid obesity had history of obstructive sleep apnea, and 2 patients showed evidence of hypercarbia prior to their ICU admission.
Determinants of Outcome
There was no significant difference in the APACHE II scores of
critically ill morbidly obese patients (19.1 ± 7.6) compared to the
nonobese group (20.6 ± 12.2) [p = 0.6]. The APACHE II scores of
survivors for the morbidly obese and the nonobese group were
16.3 ± 4.7 and 14.9 ± 8.2, respectively, while the APACHE II
scores for nonsurvivors were 31.2 ± 10.5 and 44.1 ± 9.8
(p < 0.001 and p < 0.001, respectively). However, the predicted
mortality of survivors in the morbidly obese group was not
significantly different from nonsurvivors (27% and 41%; p = 0.09)
in contrast to the nonobese group, in which the predicted mortality of
survivors was significantly lower compared to nonsurvivors (22% and
68%; p < 0.0001). The relationship between the observed mortality
and the APACHE II predicted mortality is listed in Table 7
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Discussion |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The first objective of this study was to examine the mortality of
critically ill morbidly obese patients admitted to the medical ICU
compared to a group of nonobese patients. The results of our series of
249 patients indicated a significant increase in mortality for those
patients with BMI 40 kg/m2 compared to those
with BMI < 30 kg/m2. This was not surprising
given the higher number of comorbidities in the morbidly obese group
known to be associated with poor prognosis. Numerous epidemiologic
studies have pointed to the association between mortality and
increasing BMI in all age groups and for all categories of
death.14
15
16
The adverse effect of weight on longevity was
clearly demonstrated in the Framingham study,14
in which
the mortality rate for overweight nonsmoking men was 3.9 times higher
than those for nonsmoking who were at desirable weight. Yet, outcome
data from critically ill morbidly obese patients are not widely
available. There have been only a limited number of studies addressing
ICU mortality of critically ill obese patients; the majority reflects
the surgical experience. Smith-Choban and colleagues17
reviewed the records of 184 patients with blunt trauma. The observed
mortality for those with BMI > 31 kg/m2 was
42.1% compared to 5% and 8% for the average (BMI, < 27
kg/m2) and the overweight (BMI, 27 to 31
kg/m2), although the groups did not differ in
age, injury severity score, or time of mechanical ventilation.
Respiratory failure attributed to ARDS was the primary factor
responsible for the increased mortality in that group. A similar
conclusion was also reported in patients undergoing liver
transplantation, for whom morbid obesity was associated with increased
incidence of wound infection and early death from multisystem organ
failure.18
In this context, one of the significant findings of this study relates to the impact of morbid obesity on the respiratory system. The prolonged time of mechanical ventilation and the higher oxygen requirement reflect the myriad of physiologic alterations in pulmonary function described in obese subjects. Studies19 20 of conventional respiratory function tests have uniformly showed a reduction in functional residual capacity due to the effect of abdominal contents on the diaphragm. This leads to a reduced expiratory volume in the face of a fixed residual volume. In consequence, ventilation at the lung bases is diminished causing a pronounced ventilation perfusion abnormality, and arterial hypoxemia, particularly in the supine position.21 22 Vaughan and coworkers23 have noted that obese patients have a significant preoperative reduction in PaO2 that tends to worsen during and in the postoperative phase.
Liberation from mechanical ventilation is also delayed in morbidly
obese patients due to increased work of breathing resulting from
increased airway resistance, abnormal chest elasticity, and
inefficiency of the respiratory muscles. Sharp and
associates24
have shown that the mechanical work needed to
passively ventilate subjects weighing 114 kg is two to four times
that required for lighter individuals. The extra work in moving the
chest is attributed to a decrease in chest wall compliance associated
with the obese subject’s accumulation of fat in and around the ribs,
the diaphragm, and the abdomen.25
Burns and
colleagues26
have suggested that the reverse Trendelenburg
position at 45° can facilitate the weaning process by allowing a
larger tidal volume and lower respiratory rate.
Because of the altered drug pharmacokinetics associated with obesity, the observed differences in ventilatory period and weaning time could be explained potentially by the type or the extended effect of sedatives used during the course of the ICU stay. In particular, benzodiazepines are widely distributed throughout body tissues because of their high lipophilicity. Elimination half-lives and their active metabolites are usually prolonged, and dosing recommendations for these drugs in this subset of population are often nonexistent. In the current study, sedation was maintained primarily with lorazepam, making unlikely that the observed differences in duration of mechanical ventilation and weaning trials were related to the use of different type of sedatives. Nevertheless, further prospective investigations are needed to define the optimal usage and appropriate monitoring of sedation of the critically ill morbidly obese patient.
Our multivariate analysis has indicated that the PaO2/FIO2 ratio of < 200 for > 48 h is an independent risk factor for mortality. Several investigators have emphasized that statistical comparisons of the PaO2/FIO2 ratio of ARDS survivors and nonsurvivors were not significant on the first day,27 28 and these reports are consistent with our univariate analysis where the mean PaO2/FIO2 in the first 24 h of survivors was 181 ± 67 and 159 ± 52 in the obese nonsurvivors, respectively (p = 0.4). Bone and colleagues29 found, however, that the PaO2/FIO2 ratio became significantly higher in survivors only after > 24 h of conventional mechanical ventilation.
Complications from indwelling vascular catheters in the morbidly obese group have been considered to occur more frequently than the nonobese group. The loss of anatomic landmarks, and the increase in the depth of insertion to access venipuncture have been cited as potential reasons for catheter malposition, and local puncture complications. Yet, there has been no well-designed comparative study, to our knowledge, to address the rate of complication from central venous catheters in this particular group. In the current study, we found no significant difference in complications attributed to the cannulation of the central venous circulation between the two groups although the subclavian and the internal jugular vein catheterization were more commonly attempted in the morbidly obese group (82% vs 62% in the nonobese group). The use of a small-bore "locator" needle30 31 and the application of Doppler ultrasound-guided technique are likely to have contributed to the low complication rates. Similarly, the rate of infectious complications was not significantly different between the two groups even though there was a trend toward a higher rate of infection in the morbidly obese group. It is thought that to the greater number of skin punctures during catheter insertion and particularly, the extended duration of catheterization in the obese group are plausible explanation for this observation.
Objective and accurate estimation of outcome is needed more than ever, particularly in a high-risk and high-cost environments such as the ICU. The APACHE III,32 the simplified acute physiologic score II,33 and the mortality probability model II34 represent the most current and updated scoring systems available to predict mortality for adult ICU patients. All these scores were developed using large patient databases. Yet, morbid obesity was not considered in the list of comorbid variables in the development of these scoring systems. Thus, their prediction may be effective only in patients from cohorts similar to those in the original database. The lack of difference between the predicted mortality of survivors and nonsurvivors in the morbidly obese group albeit a significant variance in the APACHE scores emphasizes the concept that differences in patient demographics may influence the behavior of these predictive models,35 36 and underscores the need for a multicenter study to assess the accuracy of these models in predicting outcome of critically ill morbidly obese patients.
We acknowledge that the study has several limitations that warrant
further discussion. First, the control subjects were not selected
necessarily in close temporal proximity to the morbidly obese patients;
however, they were evenly distributed across the time span of the study
period, which might balance seasonal variations or changes in ICU
treatments. Second, this was a retrospective study, with all the
inherent methodologic problems associated with this type of evaluation
of clinical data. Yet, the value indicated that interobserver
variability was unlikely to have contributed to the significant
differences between the two cohorts. Third, individual differences in
ICU practices and variation in interhospital policies could not be
excluded as potential confounding factors for the observed differences
in ICU related data. These individual differences are usually related
to varying thresholds applied by physicians in their approach to
mechanical ventilation, weaning trials, and their use of invasive
procedures. Fourth, the size of the study population was relatively
small to assess a dose-response correlation between BMI and mortality,
but this is the largest study, to our knowledge, to address the impact
of morbid obesity on ICU outcome. Finally, an inescapable limitation of
any outcome study is the dynamic nature of the system that makes the
observed outcome vulnerable to change in response to new treatment
modalities.
In conclusion, we have presented the first report of ICU outcome in critically ill morbidly obese patients compared to a group of nonobese patients. We have observed a substantially higher mortality in these patients and have identified several variables independently associated with mortality. With the rising prevalence of obesity in the US population, future research should focus on implementing strategies designed to reduce organ dysfunction and long-term complications during ICU stay.
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Footnotes |
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This study was supported by a grant from the Research for Health in Erie County.
Received for publication October 13, 2000. Accepted for publication June 1, 2001.
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