My patient with diabetes mellitus is now admitted with pneumonia. Does diabetes increase the risk of pneumonia requiring hospitalization?

The weight of the evidence to date suggests that diabetes mellitus (DM) does increase the risk of pneumonia-related hospitalization.1-3

A large population-based study involving over 30,000 patients found an adjusted relative risk (RR) of hospitalization with pneumonia of 1.26 (95% C.I 1.2-1.3) among patients with DM compared to non-diabetics.  Of note, the risk of pneumonia-related hospitalization was significantly higher in type 1 as well as type 2 DM and among patients whose A1C level was ≥9.1  Another population-based study found a high prevalence of DM (25.6%) in patients hospitalized with CAP, more than double that in the population studied.2  A 2016 meta-analysis of observational studies also found increased incidence of respiratory tract infections among patients with diabetes (OR 1.35, 95% C.I. 1.3-1.4).

Not only does DM increase the risk of pneumonia-related hospitalization, but it also appears to adversely affect its outcome with increased in-hospital mortality.2 Among patients with type 2 DM,  excess mortality has also been reported at 30 days, 90 days and 1 year following hospitalization for pneumonia. 4,5 More specifically, compared to controls with CAP, 1 year mortality of patients with DM was 30% (vs 17%) in 1 study. 4

Potential reasons for the higher incidence of pneumonia among patients with DM include increased risk of aspiration (eg, in the setting of gastroparesis, decreased cough reflex), impaired immunity (eg, chemotaxis, intracellular killing), pulmonary microangiopathy and coexisting morbidity. 1,3,5,6

Bonus Pearl: Did you know that worldwide DM has reached epidemic levels, such that if DM were a nation, it would surpass the U.S. as the 3rd most populous country! 7

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References

  1. Kornum JB, Thomsen RW, RUS A, et al. Diabetes, glycemic control, and risk of hospitalization with pneumonia. A population-based case-control study. Diabetes Care 2008;31:1541-45. https://www.ncbi.nlm.nih.gov/pubmed/17595354
  2. Martins M, Boavida JM, Raposo JF, et al. Diabetes hinders community-acquired pneumonia outcomes in hospitalized patients. BMJ Open Diabetes Research and Care 2016;4:e000181.doi:10.1136/bmjdrc-2015000181. https://drc.bmj.com/content/4/1/e000181
  3. Abu-Ahour W, Twells L, Valcour J, et al. The association between diabetes mellitus and incident infections: a systematic review and meta-analysis of observational studies. BMJ Open Diabetes Research and Care 2017;5:e000336. https://drc.bmj.com/content/5/1/e000336. 
  4. Falcone M, Tiseo G, Russo A, et al. Hospitalization for pneumonia is associated with decreased 1-year survival in patients with type 2 diabetes. Results from a prospective cohort study. Medicine 2016;95:e2531. https://www.ncbi.nlm.nih.gov/pubmed/26844461
  5. Kornum JB, Thomsen RW, Rus A, et al. Type 2 diabetes and pneumonia outcomes. A population-based cohort study. Diabetes Care 2007;30:2251-57. https://www.ncbi.nlm.nih.gov/pubmed/17595354
  6. Koziel H, Koziel MJ. Pulmonary complications of diabetes mellitus. Pneumonia. Infect Dis Clin North Am 1995;9:65-96. https://www.ncbi.nlm.nih.gov/pubmed/7769221
  7. Zimmet PZ. Diabetes and its drivers: the largest epidemic in human history? Clinical Diabetes and Endocrinology 2017;3:1 https://clindiabetesendo.biomedcentral.com/articles/10.1186/s40842-016-0039-3  

 

My patient with diabetes mellitus is now admitted with pneumonia. Does diabetes increase the risk of pneumonia requiring hospitalization?

When should I consider Pseudomonas aeruginosa as a cause of respiratory tract infection in my hospitalized patient with COPD exacerbation?

The most consistent risk factor for isolation of P. aeruginosa from sputum of adults with COPD is the presence of more advanced pulmonary disease (eg, FEV-1 <35%-50% of predicted value) or functional impairment (1-5).

 

Chronic corticosteroid use is also frequently cited as an important predictor of respiratory tract colonization/infection due to P. aeruginosa in patients with COPD, while the data on antibiotic use during the previous months have been conflicting (2,4). Other risk factors may include prior isolation of P. aeruginosa and hospital admission during the previous year (1).

 
A prospective study of patients hospitalized for COPD exacerbation found P. aeruginosa to be the most frequently isolated organism, growing from 26% of validated sputum samples at initial admission, followed by Streptococcus pneumoniae and Hemophilus influenzae. In the same study, bronchiectasis (present in up to 50% of patients with COPD) was not shown to be independently associated with the isolation of P. aeruginosa (1).

 
Of interest, compared to the patients without P. aeruginosa, patients hospitalized for acute exacerbation of COPD and isolation of P. aeruginosa from sputum have significantly higher mortality: 33% at 1 year, 48% at 2 years and 59% at 3 years (5).

 

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References
1. Garcia-Vidal C, Almagro P, Romani V, et al. Pseudomonas aeruginosa in patients hospitalized for COPD exacerbation: a prospective study. Eur Respir J 2009;34:1072-78. https://www.ncbi.nlm.nih.gov/pubmed/19386694
2. Murphy TF. Pseudomonas aeruginosa in adults with chronic obstructive pulmonary disease. Curr Opin Pulm Med 2009;15:138-42. https://www.ncbi.nlm.nih.gov/pubmed/19532029
3. Miravitlles M, Espinosa C, Fernandez-Laso E, et al. Relationship between bacterial flora in sputum and functional impairment in patients with acute exacerbations of COPD. Chest 1999;116:40-6. https://www.ncbi.nlm.nih.gov/pubmed/10424501
4. Murphy TF, Brauer AL, Eschberger K, et al. Pseudomonas aeruginosa in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2008;177:853-60. https://www.ncbi.nlm.nih.gov/pubmed/18202344
5. Almagro P, Silvado M, Garcia-Vidal C, et al. Pseudomonas aeruginosa and mortality after hospital admission for chronic obstructive pulmonary disease. Respiration 2012;84:36-43. https://www.karger.com/Article/FullText/331224

 

 

When should I consider Pseudomonas aeruginosa as a cause of respiratory tract infection in my hospitalized patient with COPD exacerbation?

Is checking for orthostatic hypotension less than 1 minute after standing clinically useful?

Not only can it be useful in identifying those with history of dizziness upon standing but it may also predict a higher risk of falls, fracture, syncope and mortality long term. 1

Clinicians (myself included) have often assumed that drops in blood pressure (BP) and brief feeling of light-headedness soon after active standing are too common and “physiologic” to be of clinical utility,1,2 and have often discouraged checking for orthostatic hyotension (OH) sooner than 1 minute.

However, a 2017 report involving over 11,000 middle-aged participants (Atherosclerosis Risk in Communities Study) may make us rethink our position. This prospective study  found a significant association between participant-reported history of dizziness on standing and OH (defined as a drop in BP systolic ≥20 mmHg or diastolic ≥10 mmHg) but only at 1st measurement (mean of 28.0 seconds after standing), not at subsequent ones over a 2 minute period.

The more intriguing finding was the association between OH documented < 1 minute after standing and increased risk of falls, fracture, syncope, and mortality over a median follow-up period of 23 years. Although there were limitations to the study (eg, excluding many patients likely to have more severe OH), it appears that “premature” checking for OH less than a minute after standing  may not be useless!

Most, including the CDC, agree that rechecking the BP at 3 minutes is still indicated to identify those with sustained or delayed OH. 2,3

Also go to a related P4P post: https://pearls4peers.com/2015/12/14/how-can-i-be-sure-that-my-patient-truly-has-orthostatic-hypotension-oh/

References

  1. Juraschek SP, Daya N, Rawlings AM, et al. Comparison of early versus late orthostatic hypotension assessment times in middle-age adults. JAMA Intern Med 2017;1177:1316-1323. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661881/
  2. Singer W, Low PA. Early orthostatic hypotension and orthostatic intolerance-more than an observation or annoyance. JAMA Intern Med 2017;1177:1234-25. https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2645144
  3.  CDC. https://www.cdc.gov/steadi/pdf/measuring_orthostatic_blood_pressure-a.pdf. Accessed February 7, 2017.

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Is checking for orthostatic hypotension less than 1 minute after standing clinically useful?

Why are patients with cirrhosis and upper gastrointestinal bleed routinely treated with antibiotics?

Cirrhotic patients with upper gastrointestinal bleed (UGIB) are at high risk of bacterial infections: 22% during the first 48 h after admission, 35-66% within 2 weeks of initial bleeding1. Antibiotic prophylaxis has been shown to reduce short term mortality, bacterial infections, early rebleeding and volume of blood transfused1-4.

But what is the exact connection between UGIB and bacterial infections in cirrhosis? One hypothesis is that UGIB sets up the host for bacterial infection via translocation (eg, due to hypovolemia), procedures necessary in the management of bleeding (eg endoscopy, sclerotherapy, IV access), and aspiration pneumonia. More intriguing is the reverse hypothesis—that is the bacterial infection serves as a trigger for UGIB.  Several lines of evidence support this view1,2.

  • Cirrhotic patients admitted for non-UGIB-related conditions may be 4x more likely to develop UGIB during their hospitalization in the presence of bacterial infection on admission4
  • Infections predispose to early variceal rebleeding
  • Infection/endotoxemia increase portal pressure, and impair liver function and coagulation
  • Commonly cited risk factors for variceal bleeding (eg, hepatic venous pressure gradient, liver function, size of varices) do not readily explain why bleeding occurs unpredictably and why despite daily increases in portal pressure (eg, following daily meals and exercises), UGIB is relatively infrequent.

 

References

  1. Thalheimer U, Triantos CK, Samonakis DN, et al. Infection, coagulation, and variceal bleeding in cirrhosis. Gut 2005;54:556-63. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774431
  2. Goulis J. Bacterial infection in the pathogenesis of variceal bleeding. Is there any role for antibiotic prophylaxis in the cirrhotic patient. Ann Gastroenterol 2001;14:205-11. http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=4&ved=0ahUKEwjNh-rhlpLVAhXGdD4KHSurANcQFgg4MAM&url=http%3A%2F%2Fwww.annalsgastro.gr%2Findex.php%2Fannalsgastro%2Farticle%2Fdownload%2F80%2F71&usg=AFQjCNHJfAyYAjuNXpwsWGrVuyuxxgJYKg
  3. Soares-Weiser K, Brezis, Tur-Kaspa R, et al. Antibiotic prophylaxis of bacterial infections in cirrhotic inpatients: a meta-analysis of randomized controlled trials. Scand J Gastroenterol 2003;38:193-200. http://www.tandfonline.com/doi/abs/10.1080/00365520310000690
  4. Anastasioua J, Williams R. When to use antibiotics in the cirrhotic patient? The evidence base. Ann Gastroenterol. 2013; 26(2): 128–131. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3959942
  5. Benavides J, Fernandez N, Colombato L, et al. Further evidence linking bacterial infection and upper G.I. bleeding in cirrhosis. Results from a large multicentric prospective survey in Argentina. J Hepatol 2003;38 (suppl 2):A176. http://www.journal-of-hepatology.eu/article/S0168-8278(03)80592-5/abstract

 

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Why are patients with cirrhosis and upper gastrointestinal bleed routinely treated with antibiotics?

Can syncope be related to acute pulmonary embolism in the absence of hemodynamic instability or right ventricular failure?

Although we often think of syncope caused by acute pulmonary embolism (APE) in the setting of submassive or massive APE and right ventricular failure or shock (1,2), less massive APE may potentially cause syncope as well by triggering a vaso-vagal reflex (3).

For sure, a significant association between submassive or massive APE and syncope has been reported (1,2).  More specifically, patients with syncope and APE may be more likely to have systolic blood pressure <90 mmHg, right ventricular dilation and right ventricular hypokinesis (1). Another study reported a higher rate of central embolism (83% vs 43%), right ventricular dysfunction (91% vs 68%) and troponin positivity (80% vs 39%), but not 30 day mortality (2).

In contrast, 1 study found that patients with syncope as a presenting symptom of APE did not show a more serious clinical picture (e.g. shock) than those without syncope (3), while another found EKG signs of acute right ventricle overload in only 25% of patients with syncope (4).  

So while massive APEs may be associated with syncope, they don’t seem to be a prerequisite for this condition.

References

1.  Omar HR, Mirsaeidi M, Weinstock MB, et al. Syncope on presentation is a surrogate for submassive and massive acute pulmonary embolism. Am J Emerg Med 2018;36:297-300. https://www.ncbi.nlm.nih.gov/pubmed/29146419

2. Altinsoy B, Erboy F, Tanriverdi H, et al. Syncope as a presentation of acute pulmonary embolism. Ther Clin Risk Manag 2016;12:1023-28. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4930221/

3. Castelli R, Tarsia P, Tantardini G et al. Syncope in patients with pulmonary embolism: comparison between patients with syncope as the presenting symptom of pulmonary embolism and patients with pulmonary embolism without syncope. Vascular Medicine 2003;8:257-261. https://journals.sagepub.com/doi/abs/10.1191/1358863x03vm510oa

4. Miniati M, Cenci, Monti S, et al. Clinical presentation of acute pulmonary embolism: survey of 800 cases. PloS One 2012;7:e30891.

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Can syncope be related to acute pulmonary embolism in the absence of hemodynamic instability or right ventricular failure?