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METHODS: Using a retrospective chart review, we examined 376 consecutive inpatient encounters with the diagnosis of pneumonia at discharge from a community teaching hospital. Patients were evaluated by age, sex, admission serum sodium, blood urea nitrogen (BUN) level, creatinine, and fluid administered in the first 48 hours of treatment. We classified these patients as either showing radiographic progression (P) or no radiographic progression (NP) by comparison of admission and follow-up radiographs.
RESULTS: A total of 125 patient encounters satisfied inclusion criteria for the study. Using the Student t test we noted a statistically significant difference between the P and NP groups for BUN level (P=.02), volume of fluid administered during the first 48 hours (P=.04), and marginally for age (P=.05). The P group had higher BUN levels (mean=34 vs 24), more 48-hour fluid intake (mean=5824 mL vs 4764 mL), and younger age (mean=59 years vs 66 years) than the NP group. Logistic regression poorly predicted which patients would have worsening infiltrate on the second radiograph.
CONCLUSIONS: Elevated admission BUN level and higher fluid volume administered in the first 48 hours of admission were associated with worsening radiographic findings of pneumonia after hydration. Prospective studies are needed for confirmation of our results.
More than 2.5 million cases of pneumonia are diagnosed each year in the United States,1 and the hospitalization rate ranges from fewer than 1 of every 1000 persons aged 35 to 44 years to more than 11 of every 1000 persons aged 75 years or older.2,3 The annual direct cost of treating pneumonia is estimated to be $14 billion, of which $8 billion is for inpatient care. Pneumonia is also responsible for $9 billion in lost wages4-6 and is the sixth leading cause of death in the United States6—and these numbers may be increasing.7,8 It is the most frequently encountered life-threatening infectious disease in the United States.9 Accurate diagnosis, treatment, and follow-up are essential for treating this serious disease.
Physicians often obtain chest radiographs in the course of evaluating acutely ill febrile patients with suspected pneumonia. Many of these patients have some degree of fluid volume depletion secondary to the effects of the acute illness, as well as chronic illnesses and concomitant medication use. It is widely believed that the radiographic findings of community-acquired pneumonia (CAP) may be masked by volume depletion and that repletion may facilitate the expression of infiltrates on posthydration chest radiographs.4 This phenomenon has been noted in a recent publication about CAP,5 and we have encountered this clinical concept in discussions with colleagues.
Unfortunately, few data are available to support or refute the concept that fluid volume status affects the radiographic findings in CAP. A MEDLINE database search of the literature from 1966 to the present involving numerous combinations of key words yielded no human studies on this subject. One case study was reported of a dehydrated older person with a normal chest radiograph on admission for suspected pneumonia who developed a lobar infiltrate after rehydration.10
Our goal for this initial retrospective study was to determine if a relation exists between initial volume depletion, repletion, and subsequent radiographic findings of CAP. This information could be useful in determining the appropriate use of repeat radiographs in the evaluation of patients with clinical pneumonia.
Methods
The hospital records of 376 consecutive inpatient encounters with the discharge diagnosis of CAP between June 1996 and June 1998 were drawn from a 500-bed community teaching hospital. We reviewed them for the following inclusion criteria: 18 years of age or older; nonpregnant; chest radiographs obtained on admission and within 96 hours of admission; and at least 2 clinical indicators to support the radiographic diagnosis of pneumonia (fever >37.8 °C, leukocytosis, tachypnea, vomiting, pleuritic pain, productive cough, positive blood cultures.). A total of 125 records met the inclusion criteria. Each of these records was evaluated for reported chest radiograph results, fluids administered during the first 24 hours (intravenous and oral), blood urea nitrogen (BUN) level, repeat BUN level after 24 to 48 hours, admission creatinine level, repeat creatinine level after 24 to 48 hours, age, sex, race, weight, and admission serum sodium level.
We grouped the patients according to reported change in chest radiographs. The progression group (P) had chest radiograph reports indicating worsening appearance of infiltrates after fluid administration. The no-progression (NP) group had reports indicating either no change or improvement in the appearance of the infiltrates after fluid administration.
All continuous variables were analyzed with a 2-sample Student t test for equal means between the P and NP groups. We used stepwise logistic regression to determine associations between potential predictor variables and between the groups. Continuous variables were graphed against the logit to access linearity, and we examined the Hosmer-Lemeshaw statistic11 to help determine adequacy of the model. We analyzed data using the PROC t test and the PROC logistic in the SAS 6.12 software.12
Results
A total of 125 records satisfied study admission criteria. Our record review revealed that 42 patients had radiographic worsening (P), and the remaining 83 had no change or improvement radiographically (NP). The cumulative data for each group is shown in [Table 1].
We found that admission BUN levels were significantly greater for the P group (mean=12.24 mmol/L [34.3 mg/dL]) than the NP group (mean=8.57 mmol/L [24.0 mg/dL]). Fluid intake during the first 48 hours after admission was also significantly greater for the P group (mean=5824.0 mL) than the NP group (mean=4764.3 mL). There was marginal significance (P=.053) between the 2 groups for age. There was no significant difference between the 2 groups for sodium levels on admission. Thus, those patients in the P group were more likely to have a higher admission BUN level, a higher fluid intake in the first 48 hours following admission, and to be younger than the NP patients.
Results of the logistic regression model showed that few factors were related to the change in radiographic findings, and no combination of factors seemed to be a good predictor for this change. The model poorly predicted which patients would show progressive radiographic infiltrates on the basis of age and admission BUN level. Although a significant difference was found between the 2 groups with respect to the first 48-hour fluid intake, this factor was dropped from the logistic regression model because it paralleled the admission BUN level [Table 2]. On the basis of a patient’s age and admission BUN level, the model could correctly predict only 28% of patients who would show progressive radiographic changes. In contrast, the same model correctly predicted 92% of patients who would show no change or improvement on subsequent radiographic studies. The c statistic (which is equivalent to the area under the curve for the receiver-operating characteristic) equals 0.68.
Discussion
The diagnosis of CAP is usually made by the presence of signs and symptoms of lower respiratory tract infection coupled with the finding of at least one acute opacity on the chest radiograph.1,13 Some clinicians believe that such an opacity is necessary for the diagnosis of CAP, and they consider it the gold standard for the diagnosis in conjunction with supporting data from the history and physical examination.2,4,5 However, radiographic and clinical findings are not always consistent. Heckerling14 found that no clinical findings other than auscultory abnormalities could be used to predict the presence of pneumonia on chest radiography. A review of the literature by Metlay and colleagues15 found that there is no reliable combination of findings that can rule in the diagnosis of pneumonia. Up to 25% of young adults may not have auscultory findings of pneumonia.4 It is well documented that elderly patients may initially manifest no fever, minimal respiratory symptoms, and minimal radiographic infiltrates despite laboratory documentation of pneumonia.16,17 Patients with neutropenia or infections with atypical organisms or viruses may not manifest an infiltrate on chest radiograph until several days after clinical symptoms appear.5,9,18 Dehydration or volume depletion has also been shown to produce this phenomenon.4,5,10
Pneumonia has been defined as inflammation and consolidation of lung tissue due to an infectious agent. When sufficient fluid has collected in the normally air-filled spaces, X-ray beam attenuation occurs and an opacity appears on a chest radiograph. It has been postulated that decreased pulmonary hydrostatic pressure and increased pulmonary oncotic pressure secondary to dehydration or volume depletion may diminish the flux of fluid into the alveoli and interstitium and thus delay or alter the radiographic findings of pneumonia.19 Cooligan and coworkers20 found that small increases in pulmonary capillary wedge pressure increased wet lung weight in euvolemic dogs with pneumococcal pneumonia, but no radiographic evaluation was performed. Caldwell and colleagues19 found that acute intravascular volume depletion did not affect the radiographic evolution of pneumococcal pneumonia in dogs, but they did not evaluate the effects of fluid volume repletion. Caldwell and coworkers also noted that on retrospective chart review of 20 consecutive human patients with pneumonia and the diagnosis of dehydration, all had an infiltrate apparent radiographically at the time of admission. The effects of rehydration were not addressed in these patients.
Our retrospective study appears to be the first to specifically address the relationship between pneumonia, hydration status, rehydration, and the effect on the radiographic appearance of pneumonia. Our results show an association between an elevated admission BUN level, volume of fluids given, and a worsening of the radiographic appearance of CAP. A future prospective study could teach us more about diagnostic strategies for CAP, including any situations in which repeated radiographs are helpful.
We were not able to address the question of whether the radiographic findings of pneumonia can be completely masked by dehydration and subsequently expressed by rehydration; our findings, however, suggest that there may be some basis for this premise.
Limitations
Our study has a number of limitations. There is an inherent selection bias in our retrospective process: Patients who received only one chest radiograph because of misdiagnosis, management decision, or other reasons were excluded from the study. Follow-up chest radiographs within a few days are generally not indicated and are not obtained in clinically stable patients who may only show worsening or improving patterns on radiograph.6,13 Also, the retrospective nature of the study precluded the collection of a uniform database or uniform evaluation of possible etiologic agents. Viral and mycoplasma pneumonias are well documented to have a lag between onset of symptoms and evolution of radiographic findings,9 that may have led to inappropriate group assignment or complete exclusion from the study. The determination of the presence, progression, or nonprogression of radiographic findings is somewhat subjective and may affect our results. Our data are based on the reported radiograph interpretation from a randomly assigned radiologist. Interobserver agreement between radiologists for the determination of infiltrates on chest radiographs was found to be only 80% in a recent study.21 Finally, hydration status was difficult to determine. Although the BUN level was significantly higher in the P group than in the NP group, BUN level is not a specific marker for dehydration or intravascular volume status. The higher serum sodium levels of the P group, while not achieving statistical significance, may have been a better marker of total body water status. Although fluid volume depletion and dehydration are very different clinical problems,22 the determination of which condition was present, and the severity of that condition, was not possible in our study. Although statistically significant, the difference in fluid intake between the 2 groups may not be clinically significant. Furthermore, dehydration alone has been shown to adversely affect lung host defense in rats.23 If applicable to humans, this could also unexpectedly affect our results.
Conclusions
To our knowledge, this study is the first to try to define the relationship of fluid volume status and radiographic progression of CAP in humans. The retrospective nature of our study leads to several limitations and potential sources of bias, but it appears to show that there is a correlation between markers of fluid volume status, hydration, and the evolution of the radiographic findings. A prospective clinical study is needed to further define this relationship.
Acknowledgments
Our work was funded by a grant from the Clinical Research Center of the Medical Center of Central Georgia. We wish to thank Jennifer K. Rayhill for her assistance in preparing this manuscript.
1. MN. Approach to the patient with pulmonary infections. In: Fishman AP, ed. Fishman’s pulmonary diseases and disorders. 3rd ed. New York, NY: McGraw-Hill; 1998.
2. TJ. Acute bronchitis and community-acquired pneumonia. In: Fishman AP, ed. Fishman’s pulmonary diseases and disorders. 3rd ed. New York, NY: McGraw-Hill; 1998.
3. RA. Epidemiology of community-acquired respiratory tract infections in adults. Am J Med 1985;78:(suppl):32-37.
4. TJ. Community-acquired pneumonia. Clinical Infect Dis 1994;18:501-15.
5. JG, Munday LM. Community-acquired pneumonia. N Engl J Med 1995;333:1618-24.
6. HA, Neiderman MS. Community-acquired pneumonia. Disease-a-month 1998;44:613-76.
7. RW, Teutsch SM, Simonsen L, Klug LA, et al. Trends in infectious disease mortality in the United States. JAMA 1996;275:189-93.
8. GL, Conn LA, Pinner RW. Trends in infectious disease mortality in the United States during the 20th century. JAMA 1999;281:61-66.
9. RS, Pare JA, Fraser RG. Synopsis of diseases of the chest. Philadelphia, Pa: WB Saunders; 1994.
10. FM, Simon M. Occult pneumonia associated with dehydration: myth or reality. Am J Radiology 1987;148:853-54.
11. DW, Lemeshow S. Applied logistic regression. New York, NY: John Wiley and Sons; 1989.
12. Institute, Inc. SAS/STAT user’s guide, version 6. 4th ed. Cary, NC: SAS Institute Inc; 1989.
13. A, Ketai L, Lotgren R. Fundamentals of chest radiology. Philadelphia, Pa: WB Saunders; 1996.
14. PS. The need for chest roentgenograms in adults with acute respiratory illness: clinical predictors. Arch Intern Med 1986;146:1321-24.
15. JP, Kapoor WN, Fine MJ. Does this patient have community-acquired pneumonia? Diagnosing pneumonia by history and physical examination. JAMA 1997;278:1440-45.
16. R, Tornes A, El-Ebiary M, Mensa J, Estruch R, Ruiz M, Angrill J, Soler N. Community-acquired pneumonia in the elderly: clinical and nutritional aspects. Am J Resp Crit Care Med 1997;156:1908-14.
17. RL, Peterson PK. Immunodeficiency of the elderly. Rev Infect Dis 1987;9:1127-39.
18. GR, Herman C, Pope T, Stowart MF. The role of the chest roentgenogram in febrile neutropenic patients. Arch Intern Med 1991;151:701-04.
19. A, Glauser FL, Smith WR, Hoshiko M, Morton, ME. The effects of dehydration on the radiographic and pathologic appearance of experimental canine segmental pneumonia. Am Rev Resp Dis 1975;112:651-56.
20. T, Light RB, Wood LD, Mink SN. Plasma volume expansion in canine pneumococcal pneumonia: its effects on respiratory gas exchange and pneumonia size. Am Review Resp Dis 1982;126:86-91.
21. MN, Hill LC, Murphy M, et al. Interobserver reliability of the chest radiograph in community-acquired pneumonia. Chest 1996;110:343-50.
22. K, Matsuura D, Cizman B, et al. Language guiding therapy: the case of dehydration versus volume depletion. Ann Intern Med 1997;127:848-53.
23. JF, La Force FM, Huber GL. Variations in lung water and pulmonary host defense mechanisms. Am Surg 1973;39:630-36.
METHODS: Using a retrospective chart review, we examined 376 consecutive inpatient encounters with the diagnosis of pneumonia at discharge from a community teaching hospital. Patients were evaluated by age, sex, admission serum sodium, blood urea nitrogen (BUN) level, creatinine, and fluid administered in the first 48 hours of treatment. We classified these patients as either showing radiographic progression (P) or no radiographic progression (NP) by comparison of admission and follow-up radiographs.
RESULTS: A total of 125 patient encounters satisfied inclusion criteria for the study. Using the Student t test we noted a statistically significant difference between the P and NP groups for BUN level (P=.02), volume of fluid administered during the first 48 hours (P=.04), and marginally for age (P=.05). The P group had higher BUN levels (mean=34 vs 24), more 48-hour fluid intake (mean=5824 mL vs 4764 mL), and younger age (mean=59 years vs 66 years) than the NP group. Logistic regression poorly predicted which patients would have worsening infiltrate on the second radiograph.
CONCLUSIONS: Elevated admission BUN level and higher fluid volume administered in the first 48 hours of admission were associated with worsening radiographic findings of pneumonia after hydration. Prospective studies are needed for confirmation of our results.
More than 2.5 million cases of pneumonia are diagnosed each year in the United States,1 and the hospitalization rate ranges from fewer than 1 of every 1000 persons aged 35 to 44 years to more than 11 of every 1000 persons aged 75 years or older.2,3 The annual direct cost of treating pneumonia is estimated to be $14 billion, of which $8 billion is for inpatient care. Pneumonia is also responsible for $9 billion in lost wages4-6 and is the sixth leading cause of death in the United States6—and these numbers may be increasing.7,8 It is the most frequently encountered life-threatening infectious disease in the United States.9 Accurate diagnosis, treatment, and follow-up are essential for treating this serious disease.
Physicians often obtain chest radiographs in the course of evaluating acutely ill febrile patients with suspected pneumonia. Many of these patients have some degree of fluid volume depletion secondary to the effects of the acute illness, as well as chronic illnesses and concomitant medication use. It is widely believed that the radiographic findings of community-acquired pneumonia (CAP) may be masked by volume depletion and that repletion may facilitate the expression of infiltrates on posthydration chest radiographs.4 This phenomenon has been noted in a recent publication about CAP,5 and we have encountered this clinical concept in discussions with colleagues.
Unfortunately, few data are available to support or refute the concept that fluid volume status affects the radiographic findings in CAP. A MEDLINE database search of the literature from 1966 to the present involving numerous combinations of key words yielded no human studies on this subject. One case study was reported of a dehydrated older person with a normal chest radiograph on admission for suspected pneumonia who developed a lobar infiltrate after rehydration.10
Our goal for this initial retrospective study was to determine if a relation exists between initial volume depletion, repletion, and subsequent radiographic findings of CAP. This information could be useful in determining the appropriate use of repeat radiographs in the evaluation of patients with clinical pneumonia.
Methods
The hospital records of 376 consecutive inpatient encounters with the discharge diagnosis of CAP between June 1996 and June 1998 were drawn from a 500-bed community teaching hospital. We reviewed them for the following inclusion criteria: 18 years of age or older; nonpregnant; chest radiographs obtained on admission and within 96 hours of admission; and at least 2 clinical indicators to support the radiographic diagnosis of pneumonia (fever >37.8 °C, leukocytosis, tachypnea, vomiting, pleuritic pain, productive cough, positive blood cultures.). A total of 125 records met the inclusion criteria. Each of these records was evaluated for reported chest radiograph results, fluids administered during the first 24 hours (intravenous and oral), blood urea nitrogen (BUN) level, repeat BUN level after 24 to 48 hours, admission creatinine level, repeat creatinine level after 24 to 48 hours, age, sex, race, weight, and admission serum sodium level.
We grouped the patients according to reported change in chest radiographs. The progression group (P) had chest radiograph reports indicating worsening appearance of infiltrates after fluid administration. The no-progression (NP) group had reports indicating either no change or improvement in the appearance of the infiltrates after fluid administration.
All continuous variables were analyzed with a 2-sample Student t test for equal means between the P and NP groups. We used stepwise logistic regression to determine associations between potential predictor variables and between the groups. Continuous variables were graphed against the logit to access linearity, and we examined the Hosmer-Lemeshaw statistic11 to help determine adequacy of the model. We analyzed data using the PROC t test and the PROC logistic in the SAS 6.12 software.12
Results
A total of 125 records satisfied study admission criteria. Our record review revealed that 42 patients had radiographic worsening (P), and the remaining 83 had no change or improvement radiographically (NP). The cumulative data for each group is shown in [Table 1].
We found that admission BUN levels were significantly greater for the P group (mean=12.24 mmol/L [34.3 mg/dL]) than the NP group (mean=8.57 mmol/L [24.0 mg/dL]). Fluid intake during the first 48 hours after admission was also significantly greater for the P group (mean=5824.0 mL) than the NP group (mean=4764.3 mL). There was marginal significance (P=.053) between the 2 groups for age. There was no significant difference between the 2 groups for sodium levels on admission. Thus, those patients in the P group were more likely to have a higher admission BUN level, a higher fluid intake in the first 48 hours following admission, and to be younger than the NP patients.
Results of the logistic regression model showed that few factors were related to the change in radiographic findings, and no combination of factors seemed to be a good predictor for this change. The model poorly predicted which patients would show progressive radiographic infiltrates on the basis of age and admission BUN level. Although a significant difference was found between the 2 groups with respect to the first 48-hour fluid intake, this factor was dropped from the logistic regression model because it paralleled the admission BUN level [Table 2]. On the basis of a patient’s age and admission BUN level, the model could correctly predict only 28% of patients who would show progressive radiographic changes. In contrast, the same model correctly predicted 92% of patients who would show no change or improvement on subsequent radiographic studies. The c statistic (which is equivalent to the area under the curve for the receiver-operating characteristic) equals 0.68.
Discussion
The diagnosis of CAP is usually made by the presence of signs and symptoms of lower respiratory tract infection coupled with the finding of at least one acute opacity on the chest radiograph.1,13 Some clinicians believe that such an opacity is necessary for the diagnosis of CAP, and they consider it the gold standard for the diagnosis in conjunction with supporting data from the history and physical examination.2,4,5 However, radiographic and clinical findings are not always consistent. Heckerling14 found that no clinical findings other than auscultory abnormalities could be used to predict the presence of pneumonia on chest radiography. A review of the literature by Metlay and colleagues15 found that there is no reliable combination of findings that can rule in the diagnosis of pneumonia. Up to 25% of young adults may not have auscultory findings of pneumonia.4 It is well documented that elderly patients may initially manifest no fever, minimal respiratory symptoms, and minimal radiographic infiltrates despite laboratory documentation of pneumonia.16,17 Patients with neutropenia or infections with atypical organisms or viruses may not manifest an infiltrate on chest radiograph until several days after clinical symptoms appear.5,9,18 Dehydration or volume depletion has also been shown to produce this phenomenon.4,5,10
Pneumonia has been defined as inflammation and consolidation of lung tissue due to an infectious agent. When sufficient fluid has collected in the normally air-filled spaces, X-ray beam attenuation occurs and an opacity appears on a chest radiograph. It has been postulated that decreased pulmonary hydrostatic pressure and increased pulmonary oncotic pressure secondary to dehydration or volume depletion may diminish the flux of fluid into the alveoli and interstitium and thus delay or alter the radiographic findings of pneumonia.19 Cooligan and coworkers20 found that small increases in pulmonary capillary wedge pressure increased wet lung weight in euvolemic dogs with pneumococcal pneumonia, but no radiographic evaluation was performed. Caldwell and colleagues19 found that acute intravascular volume depletion did not affect the radiographic evolution of pneumococcal pneumonia in dogs, but they did not evaluate the effects of fluid volume repletion. Caldwell and coworkers also noted that on retrospective chart review of 20 consecutive human patients with pneumonia and the diagnosis of dehydration, all had an infiltrate apparent radiographically at the time of admission. The effects of rehydration were not addressed in these patients.
Our retrospective study appears to be the first to specifically address the relationship between pneumonia, hydration status, rehydration, and the effect on the radiographic appearance of pneumonia. Our results show an association between an elevated admission BUN level, volume of fluids given, and a worsening of the radiographic appearance of CAP. A future prospective study could teach us more about diagnostic strategies for CAP, including any situations in which repeated radiographs are helpful.
We were not able to address the question of whether the radiographic findings of pneumonia can be completely masked by dehydration and subsequently expressed by rehydration; our findings, however, suggest that there may be some basis for this premise.
Limitations
Our study has a number of limitations. There is an inherent selection bias in our retrospective process: Patients who received only one chest radiograph because of misdiagnosis, management decision, or other reasons were excluded from the study. Follow-up chest radiographs within a few days are generally not indicated and are not obtained in clinically stable patients who may only show worsening or improving patterns on radiograph.6,13 Also, the retrospective nature of the study precluded the collection of a uniform database or uniform evaluation of possible etiologic agents. Viral and mycoplasma pneumonias are well documented to have a lag between onset of symptoms and evolution of radiographic findings,9 that may have led to inappropriate group assignment or complete exclusion from the study. The determination of the presence, progression, or nonprogression of radiographic findings is somewhat subjective and may affect our results. Our data are based on the reported radiograph interpretation from a randomly assigned radiologist. Interobserver agreement between radiologists for the determination of infiltrates on chest radiographs was found to be only 80% in a recent study.21 Finally, hydration status was difficult to determine. Although the BUN level was significantly higher in the P group than in the NP group, BUN level is not a specific marker for dehydration or intravascular volume status. The higher serum sodium levels of the P group, while not achieving statistical significance, may have been a better marker of total body water status. Although fluid volume depletion and dehydration are very different clinical problems,22 the determination of which condition was present, and the severity of that condition, was not possible in our study. Although statistically significant, the difference in fluid intake between the 2 groups may not be clinically significant. Furthermore, dehydration alone has been shown to adversely affect lung host defense in rats.23 If applicable to humans, this could also unexpectedly affect our results.
Conclusions
To our knowledge, this study is the first to try to define the relationship of fluid volume status and radiographic progression of CAP in humans. The retrospective nature of our study leads to several limitations and potential sources of bias, but it appears to show that there is a correlation between markers of fluid volume status, hydration, and the evolution of the radiographic findings. A prospective clinical study is needed to further define this relationship.
Acknowledgments
Our work was funded by a grant from the Clinical Research Center of the Medical Center of Central Georgia. We wish to thank Jennifer K. Rayhill for her assistance in preparing this manuscript.
METHODS: Using a retrospective chart review, we examined 376 consecutive inpatient encounters with the diagnosis of pneumonia at discharge from a community teaching hospital. Patients were evaluated by age, sex, admission serum sodium, blood urea nitrogen (BUN) level, creatinine, and fluid administered in the first 48 hours of treatment. We classified these patients as either showing radiographic progression (P) or no radiographic progression (NP) by comparison of admission and follow-up radiographs.
RESULTS: A total of 125 patient encounters satisfied inclusion criteria for the study. Using the Student t test we noted a statistically significant difference between the P and NP groups for BUN level (P=.02), volume of fluid administered during the first 48 hours (P=.04), and marginally for age (P=.05). The P group had higher BUN levels (mean=34 vs 24), more 48-hour fluid intake (mean=5824 mL vs 4764 mL), and younger age (mean=59 years vs 66 years) than the NP group. Logistic regression poorly predicted which patients would have worsening infiltrate on the second radiograph.
CONCLUSIONS: Elevated admission BUN level and higher fluid volume administered in the first 48 hours of admission were associated with worsening radiographic findings of pneumonia after hydration. Prospective studies are needed for confirmation of our results.
More than 2.5 million cases of pneumonia are diagnosed each year in the United States,1 and the hospitalization rate ranges from fewer than 1 of every 1000 persons aged 35 to 44 years to more than 11 of every 1000 persons aged 75 years or older.2,3 The annual direct cost of treating pneumonia is estimated to be $14 billion, of which $8 billion is for inpatient care. Pneumonia is also responsible for $9 billion in lost wages4-6 and is the sixth leading cause of death in the United States6—and these numbers may be increasing.7,8 It is the most frequently encountered life-threatening infectious disease in the United States.9 Accurate diagnosis, treatment, and follow-up are essential for treating this serious disease.
Physicians often obtain chest radiographs in the course of evaluating acutely ill febrile patients with suspected pneumonia. Many of these patients have some degree of fluid volume depletion secondary to the effects of the acute illness, as well as chronic illnesses and concomitant medication use. It is widely believed that the radiographic findings of community-acquired pneumonia (CAP) may be masked by volume depletion and that repletion may facilitate the expression of infiltrates on posthydration chest radiographs.4 This phenomenon has been noted in a recent publication about CAP,5 and we have encountered this clinical concept in discussions with colleagues.
Unfortunately, few data are available to support or refute the concept that fluid volume status affects the radiographic findings in CAP. A MEDLINE database search of the literature from 1966 to the present involving numerous combinations of key words yielded no human studies on this subject. One case study was reported of a dehydrated older person with a normal chest radiograph on admission for suspected pneumonia who developed a lobar infiltrate after rehydration.10
Our goal for this initial retrospective study was to determine if a relation exists between initial volume depletion, repletion, and subsequent radiographic findings of CAP. This information could be useful in determining the appropriate use of repeat radiographs in the evaluation of patients with clinical pneumonia.
Methods
The hospital records of 376 consecutive inpatient encounters with the discharge diagnosis of CAP between June 1996 and June 1998 were drawn from a 500-bed community teaching hospital. We reviewed them for the following inclusion criteria: 18 years of age or older; nonpregnant; chest radiographs obtained on admission and within 96 hours of admission; and at least 2 clinical indicators to support the radiographic diagnosis of pneumonia (fever >37.8 °C, leukocytosis, tachypnea, vomiting, pleuritic pain, productive cough, positive blood cultures.). A total of 125 records met the inclusion criteria. Each of these records was evaluated for reported chest radiograph results, fluids administered during the first 24 hours (intravenous and oral), blood urea nitrogen (BUN) level, repeat BUN level after 24 to 48 hours, admission creatinine level, repeat creatinine level after 24 to 48 hours, age, sex, race, weight, and admission serum sodium level.
We grouped the patients according to reported change in chest radiographs. The progression group (P) had chest radiograph reports indicating worsening appearance of infiltrates after fluid administration. The no-progression (NP) group had reports indicating either no change or improvement in the appearance of the infiltrates after fluid administration.
All continuous variables were analyzed with a 2-sample Student t test for equal means between the P and NP groups. We used stepwise logistic regression to determine associations between potential predictor variables and between the groups. Continuous variables were graphed against the logit to access linearity, and we examined the Hosmer-Lemeshaw statistic11 to help determine adequacy of the model. We analyzed data using the PROC t test and the PROC logistic in the SAS 6.12 software.12
Results
A total of 125 records satisfied study admission criteria. Our record review revealed that 42 patients had radiographic worsening (P), and the remaining 83 had no change or improvement radiographically (NP). The cumulative data for each group is shown in [Table 1].
We found that admission BUN levels were significantly greater for the P group (mean=12.24 mmol/L [34.3 mg/dL]) than the NP group (mean=8.57 mmol/L [24.0 mg/dL]). Fluid intake during the first 48 hours after admission was also significantly greater for the P group (mean=5824.0 mL) than the NP group (mean=4764.3 mL). There was marginal significance (P=.053) between the 2 groups for age. There was no significant difference between the 2 groups for sodium levels on admission. Thus, those patients in the P group were more likely to have a higher admission BUN level, a higher fluid intake in the first 48 hours following admission, and to be younger than the NP patients.
Results of the logistic regression model showed that few factors were related to the change in radiographic findings, and no combination of factors seemed to be a good predictor for this change. The model poorly predicted which patients would show progressive radiographic infiltrates on the basis of age and admission BUN level. Although a significant difference was found between the 2 groups with respect to the first 48-hour fluid intake, this factor was dropped from the logistic regression model because it paralleled the admission BUN level [Table 2]. On the basis of a patient’s age and admission BUN level, the model could correctly predict only 28% of patients who would show progressive radiographic changes. In contrast, the same model correctly predicted 92% of patients who would show no change or improvement on subsequent radiographic studies. The c statistic (which is equivalent to the area under the curve for the receiver-operating characteristic) equals 0.68.
Discussion
The diagnosis of CAP is usually made by the presence of signs and symptoms of lower respiratory tract infection coupled with the finding of at least one acute opacity on the chest radiograph.1,13 Some clinicians believe that such an opacity is necessary for the diagnosis of CAP, and they consider it the gold standard for the diagnosis in conjunction with supporting data from the history and physical examination.2,4,5 However, radiographic and clinical findings are not always consistent. Heckerling14 found that no clinical findings other than auscultory abnormalities could be used to predict the presence of pneumonia on chest radiography. A review of the literature by Metlay and colleagues15 found that there is no reliable combination of findings that can rule in the diagnosis of pneumonia. Up to 25% of young adults may not have auscultory findings of pneumonia.4 It is well documented that elderly patients may initially manifest no fever, minimal respiratory symptoms, and minimal radiographic infiltrates despite laboratory documentation of pneumonia.16,17 Patients with neutropenia or infections with atypical organisms or viruses may not manifest an infiltrate on chest radiograph until several days after clinical symptoms appear.5,9,18 Dehydration or volume depletion has also been shown to produce this phenomenon.4,5,10
Pneumonia has been defined as inflammation and consolidation of lung tissue due to an infectious agent. When sufficient fluid has collected in the normally air-filled spaces, X-ray beam attenuation occurs and an opacity appears on a chest radiograph. It has been postulated that decreased pulmonary hydrostatic pressure and increased pulmonary oncotic pressure secondary to dehydration or volume depletion may diminish the flux of fluid into the alveoli and interstitium and thus delay or alter the radiographic findings of pneumonia.19 Cooligan and coworkers20 found that small increases in pulmonary capillary wedge pressure increased wet lung weight in euvolemic dogs with pneumococcal pneumonia, but no radiographic evaluation was performed. Caldwell and colleagues19 found that acute intravascular volume depletion did not affect the radiographic evolution of pneumococcal pneumonia in dogs, but they did not evaluate the effects of fluid volume repletion. Caldwell and coworkers also noted that on retrospective chart review of 20 consecutive human patients with pneumonia and the diagnosis of dehydration, all had an infiltrate apparent radiographically at the time of admission. The effects of rehydration were not addressed in these patients.
Our retrospective study appears to be the first to specifically address the relationship between pneumonia, hydration status, rehydration, and the effect on the radiographic appearance of pneumonia. Our results show an association between an elevated admission BUN level, volume of fluids given, and a worsening of the radiographic appearance of CAP. A future prospective study could teach us more about diagnostic strategies for CAP, including any situations in which repeated radiographs are helpful.
We were not able to address the question of whether the radiographic findings of pneumonia can be completely masked by dehydration and subsequently expressed by rehydration; our findings, however, suggest that there may be some basis for this premise.
Limitations
Our study has a number of limitations. There is an inherent selection bias in our retrospective process: Patients who received only one chest radiograph because of misdiagnosis, management decision, or other reasons were excluded from the study. Follow-up chest radiographs within a few days are generally not indicated and are not obtained in clinically stable patients who may only show worsening or improving patterns on radiograph.6,13 Also, the retrospective nature of the study precluded the collection of a uniform database or uniform evaluation of possible etiologic agents. Viral and mycoplasma pneumonias are well documented to have a lag between onset of symptoms and evolution of radiographic findings,9 that may have led to inappropriate group assignment or complete exclusion from the study. The determination of the presence, progression, or nonprogression of radiographic findings is somewhat subjective and may affect our results. Our data are based on the reported radiograph interpretation from a randomly assigned radiologist. Interobserver agreement between radiologists for the determination of infiltrates on chest radiographs was found to be only 80% in a recent study.21 Finally, hydration status was difficult to determine. Although the BUN level was significantly higher in the P group than in the NP group, BUN level is not a specific marker for dehydration or intravascular volume status. The higher serum sodium levels of the P group, while not achieving statistical significance, may have been a better marker of total body water status. Although fluid volume depletion and dehydration are very different clinical problems,22 the determination of which condition was present, and the severity of that condition, was not possible in our study. Although statistically significant, the difference in fluid intake between the 2 groups may not be clinically significant. Furthermore, dehydration alone has been shown to adversely affect lung host defense in rats.23 If applicable to humans, this could also unexpectedly affect our results.
Conclusions
To our knowledge, this study is the first to try to define the relationship of fluid volume status and radiographic progression of CAP in humans. The retrospective nature of our study leads to several limitations and potential sources of bias, but it appears to show that there is a correlation between markers of fluid volume status, hydration, and the evolution of the radiographic findings. A prospective clinical study is needed to further define this relationship.
Acknowledgments
Our work was funded by a grant from the Clinical Research Center of the Medical Center of Central Georgia. We wish to thank Jennifer K. Rayhill for her assistance in preparing this manuscript.
1. MN. Approach to the patient with pulmonary infections. In: Fishman AP, ed. Fishman’s pulmonary diseases and disorders. 3rd ed. New York, NY: McGraw-Hill; 1998.
2. TJ. Acute bronchitis and community-acquired pneumonia. In: Fishman AP, ed. Fishman’s pulmonary diseases and disorders. 3rd ed. New York, NY: McGraw-Hill; 1998.
3. RA. Epidemiology of community-acquired respiratory tract infections in adults. Am J Med 1985;78:(suppl):32-37.
4. TJ. Community-acquired pneumonia. Clinical Infect Dis 1994;18:501-15.
5. JG, Munday LM. Community-acquired pneumonia. N Engl J Med 1995;333:1618-24.
6. HA, Neiderman MS. Community-acquired pneumonia. Disease-a-month 1998;44:613-76.
7. RW, Teutsch SM, Simonsen L, Klug LA, et al. Trends in infectious disease mortality in the United States. JAMA 1996;275:189-93.
8. GL, Conn LA, Pinner RW. Trends in infectious disease mortality in the United States during the 20th century. JAMA 1999;281:61-66.
9. RS, Pare JA, Fraser RG. Synopsis of diseases of the chest. Philadelphia, Pa: WB Saunders; 1994.
10. FM, Simon M. Occult pneumonia associated with dehydration: myth or reality. Am J Radiology 1987;148:853-54.
11. DW, Lemeshow S. Applied logistic regression. New York, NY: John Wiley and Sons; 1989.
12. Institute, Inc. SAS/STAT user’s guide, version 6. 4th ed. Cary, NC: SAS Institute Inc; 1989.
13. A, Ketai L, Lotgren R. Fundamentals of chest radiology. Philadelphia, Pa: WB Saunders; 1996.
14. PS. The need for chest roentgenograms in adults with acute respiratory illness: clinical predictors. Arch Intern Med 1986;146:1321-24.
15. JP, Kapoor WN, Fine MJ. Does this patient have community-acquired pneumonia? Diagnosing pneumonia by history and physical examination. JAMA 1997;278:1440-45.
16. R, Tornes A, El-Ebiary M, Mensa J, Estruch R, Ruiz M, Angrill J, Soler N. Community-acquired pneumonia in the elderly: clinical and nutritional aspects. Am J Resp Crit Care Med 1997;156:1908-14.
17. RL, Peterson PK. Immunodeficiency of the elderly. Rev Infect Dis 1987;9:1127-39.
18. GR, Herman C, Pope T, Stowart MF. The role of the chest roentgenogram in febrile neutropenic patients. Arch Intern Med 1991;151:701-04.
19. A, Glauser FL, Smith WR, Hoshiko M, Morton, ME. The effects of dehydration on the radiographic and pathologic appearance of experimental canine segmental pneumonia. Am Rev Resp Dis 1975;112:651-56.
20. T, Light RB, Wood LD, Mink SN. Plasma volume expansion in canine pneumococcal pneumonia: its effects on respiratory gas exchange and pneumonia size. Am Review Resp Dis 1982;126:86-91.
21. MN, Hill LC, Murphy M, et al. Interobserver reliability of the chest radiograph in community-acquired pneumonia. Chest 1996;110:343-50.
22. K, Matsuura D, Cizman B, et al. Language guiding therapy: the case of dehydration versus volume depletion. Ann Intern Med 1997;127:848-53.
23. JF, La Force FM, Huber GL. Variations in lung water and pulmonary host defense mechanisms. Am Surg 1973;39:630-36.
1. MN. Approach to the patient with pulmonary infections. In: Fishman AP, ed. Fishman’s pulmonary diseases and disorders. 3rd ed. New York, NY: McGraw-Hill; 1998.
2. TJ. Acute bronchitis and community-acquired pneumonia. In: Fishman AP, ed. Fishman’s pulmonary diseases and disorders. 3rd ed. New York, NY: McGraw-Hill; 1998.
3. RA. Epidemiology of community-acquired respiratory tract infections in adults. Am J Med 1985;78:(suppl):32-37.
4. TJ. Community-acquired pneumonia. Clinical Infect Dis 1994;18:501-15.
5. JG, Munday LM. Community-acquired pneumonia. N Engl J Med 1995;333:1618-24.
6. HA, Neiderman MS. Community-acquired pneumonia. Disease-a-month 1998;44:613-76.
7. RW, Teutsch SM, Simonsen L, Klug LA, et al. Trends in infectious disease mortality in the United States. JAMA 1996;275:189-93.
8. GL, Conn LA, Pinner RW. Trends in infectious disease mortality in the United States during the 20th century. JAMA 1999;281:61-66.
9. RS, Pare JA, Fraser RG. Synopsis of diseases of the chest. Philadelphia, Pa: WB Saunders; 1994.
10. FM, Simon M. Occult pneumonia associated with dehydration: myth or reality. Am J Radiology 1987;148:853-54.
11. DW, Lemeshow S. Applied logistic regression. New York, NY: John Wiley and Sons; 1989.
12. Institute, Inc. SAS/STAT user’s guide, version 6. 4th ed. Cary, NC: SAS Institute Inc; 1989.
13. A, Ketai L, Lotgren R. Fundamentals of chest radiology. Philadelphia, Pa: WB Saunders; 1996.
14. PS. The need for chest roentgenograms in adults with acute respiratory illness: clinical predictors. Arch Intern Med 1986;146:1321-24.
15. JP, Kapoor WN, Fine MJ. Does this patient have community-acquired pneumonia? Diagnosing pneumonia by history and physical examination. JAMA 1997;278:1440-45.
16. R, Tornes A, El-Ebiary M, Mensa J, Estruch R, Ruiz M, Angrill J, Soler N. Community-acquired pneumonia in the elderly: clinical and nutritional aspects. Am J Resp Crit Care Med 1997;156:1908-14.
17. RL, Peterson PK. Immunodeficiency of the elderly. Rev Infect Dis 1987;9:1127-39.
18. GR, Herman C, Pope T, Stowart MF. The role of the chest roentgenogram in febrile neutropenic patients. Arch Intern Med 1991;151:701-04.
19. A, Glauser FL, Smith WR, Hoshiko M, Morton, ME. The effects of dehydration on the radiographic and pathologic appearance of experimental canine segmental pneumonia. Am Rev Resp Dis 1975;112:651-56.
20. T, Light RB, Wood LD, Mink SN. Plasma volume expansion in canine pneumococcal pneumonia: its effects on respiratory gas exchange and pneumonia size. Am Review Resp Dis 1982;126:86-91.
21. MN, Hill LC, Murphy M, et al. Interobserver reliability of the chest radiograph in community-acquired pneumonia. Chest 1996;110:343-50.
22. K, Matsuura D, Cizman B, et al. Language guiding therapy: the case of dehydration versus volume depletion. Ann Intern Med 1997;127:848-53.
23. JF, La Force FM, Huber GL. Variations in lung water and pulmonary host defense mechanisms. Am Surg 1973;39:630-36.