Tag Archives: pneumonia

emDocs Cases: ED Evaluation of Community-Acquired Pneumonia

Authors: Brit Long, MD (@long_brit, EM Attending Physician at SAUSHEC) and Drew A. Long, BS (@drewlong2232, Vanderbilt University School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital)

Welcome to emDocs Cases! This will be a case-based discussion of EM topics, ranging from core to cutting edge and controversial. Today, we start with something common in emergency medicine: community-acquired pneumonia (CAP).


You start your first shift with two patients. One is a 24-year-old male with three days of fever, productive cough, and chills. He has noted decreased appetite, but no nausea, vomiting, or diarrhea. He has no past medical history, takes no medications, and has no allergies.

Exam reveals RR 23/min, HR 112 bpm, Sat 95% on RA, T 38.1C, and BP 128/68. He appears tired though nontoxic, with normal mucosa, HEENT, and abdominal exams. You detect R sided rhonchi on lung exam, but no other abnormalities.

 Your second patient is a 73-year-old female with a history of CAD and DM. She presents with three days of fever, productive cough, and chills. She lives at home with her husband, who has severe dementia. She is the primary caregiver for him. She has not been able to adequately care for him due to her illness. She takes aspirin, metoprolol, hydrochlorothiazide, and metformin.

Exam reveals RR 24/min, HR 92, Sat 90% on RA, T 37.9, and BP 132/75. She has dry mucosa, with rhonchi on the left. She has normal CV and abdominal exams as well, with no skin breakdown.

So these are our two patients. Today we will discuss several aspects of community acquired pneumonia including: 1) disease perspective, 2) history and physical exam, 3) chest radiograph, 4) alternate imaging, 5) ultrasound use, and 6) clinical scores/disposition.

1. Disease perspective: what is community acquired pneumonia?

Pneumonia is an acute infection of the pulmonary alveoli.  Pneumonia is a common infection and the leading cause of infectious deaths. The mortality rate in severe pneumonia is 28%, but it is more commonly under 5%.  The Infectious Diseases Society of America (IDSA) recently redefined pneumonia subtypes, shown here:


Community-acquired pneumonia


Acute pulmonary infection in a patient who is not hospitalized or residing in a long-term care facility 14 or more days before presentation.
Hospital-acquired pneumonia Pneumonia occurring 48 hours or more after a hospital admission not present on initial presentation.
Ventilator-associated pneumonia Pneumonia occurring 48-72 hours after intubation that wasn’t present prior to that intubation.

Community acquired pneumonia is common, as it is responsible for 60,000 hospitalizations per year.  Causes of pneumonia include bacteria (most common), viruses, and fungi. However, a microbial agent is never identified in over 50% of patients with pneumonia. Typical agents include S. pneumoniae and H. influenza, with S. pneumo being the most common. “Atypical” pathogens include Legionella, Mycoplasma, and Chlamydia. Viral causes include influenza, parainfluenza, coronavirus, and many others.

2. For our patients, what historical and physical examination findings point toward pneumonia?

The common signs and symptoms of pneumonia include cough (79%-91%), fever (up to 80%), increased sputum (up to 65%), pleuritic chest pain (up to 50%), respiratory rate above 24 breaths/minute (45% to 70%), chills (40% to 50%), and dyspnea (approximately 70%).14-20  However, no combination is diagnostic.  Lung findings like percussion and crackles are most reliable. But, as most of us know, examination varies and is not consistent between providers.11,14-18,20 

Finding Positive Likelihood Ratio Negative Likelihood Ratio













Dullness to percussion

Decreased breath sounds























Elevated WBC





The 24-year-old male clinically appears to have pneumonia. However, the older female does not have a fever. Could this still be pneumonia?

Atypical equals typical in the elderly. Patients who present with nonspecific complaints, such as altered mental status or nausea/vomiting, include elderly, immunocompromised, and debilitated patients.  Other nonspecific symptoms include lightheadedness, malaise, weakness, headache, joint pain, and rash. Older patients often have fewer symptoms, with delirium being more common. Up to 2/3 of elderly patients will not have cough, fever, or shortness of breath, and they are less likely to present with chills. 21-24 Over half will present with confusion. Respiratory rate is important to assess, as tachypnea is a reliable factor in pneumonia diagnosis. 21-24  

3. What testing is warranted? Does everyone need a CXR to diagnose pneumonia?

Clinically, the 23-year-old male has pneumonia. You have started 1 L NS, with 1 g ceftriaxone for community acquired pneumonia with 500 mg azithromycin PO. Though he meets sepsis criteria based on SIRS, he appears nontoxic and well. Does he need a CXR? Will it change your management?

 The diagnosis of CAP is typically based on the combination of history, exam, and CXR.5,6,11,13  In the ED, many patients with respiratory complaints receive a CXR, and if suggestive of pneumonia, antibiotics are often given.15-19  The prevalence of pneumonia in patients with URI symptoms approaches 5%-7% when vital signs are otherwise normal.

How good is CXR for diagnosing pneumonia?

CXR is often considered a standard for diagnosis of pneumonia, but this test lacks specificity and sensitivity. 15,16,20 The 2007 IDSA guidelines recommend some form of imaging, with clinical symptoms, to diagnose pneumonia (Level III evidence, moderate recommendation).6 However, CXR is negative in over 30% of patients with pneumonia, with a sensitivity ranging from 46%-77%.19,25-28  One study found CXR missed one third of pneumonias, and CT excluded pneumonia in 30% of cases where pneumonia was diagnosed based on CXR.20,25-28 CXR cannot be relied on for diagnosis, and many other conditions may demonstrate radiograph findings that mimic pneumonia. Immunosuppression, dehydration, and elderly patients more commonly do not demonstrate radiographic findings due to lack of neutrophil migration. 27-30 These patients may present later with radiographic findings on repeat imaging.  Other patients with influenza, pertussis, asthma, and COPD present similarly to pneumonia with negative radiograph.11  Strep pneumoniae classically presents as lobar infiltrate, Staph aureus as abscess or extensive infiltration, and Klebsiella as lobar pneumoina with bulging minor fissure. These are just several examples of “classic” findings, but these should not be relied on.

 Other findings on CXR include pleural effusions, basilar infiltrates, interstitial infiltrates, or abscesses. Pneumonia can present with varying patterns on CXR, and many patients may not demonstrate the classic radiologic findings, particularly elderly and immunocompromised patients.11,15

When is chest radiograph not warranted?

We know that history and physical exam are not always reliable. Some form of imaging, usually CXR, is often used to evaluate for pneumonia.16,23 Patients with abnormal vital signs or signs of sepsis (including tachycardia, respiratory rate > 20 breaths/minute, or fever), age greater than 64 years, and exam findings (focal consolidation, egophony, rales, rhonchi, or wheezes unilaterally) warrant radiograph.16,23,36,39-41 Patients younger than 64 years with the absence of abnormal vital signs or physical examination findings may not need CXR, as probability of pneumonia is less than 5%.16,36,41-44  Despite this, many institutional and provider preferences vary.

You obtain a CXR for both patients, as the younger male meets SIRS criteria with positive findings on exam, and the older patient has an abnormal exam. The CXR in the male is positive for right lower lobe pneumonia, and labs show WBC 12, BUN 22 mg/dL, and normal electrolytes otherwise. His lactate is 1.2. The female has nonspecific findings with negative CXR. Her lactate is 2.8, WBC is 15.2, influenza rapid screen is negative, and BUN 32 mg/dL. You are still suspicious of pneumonia based on her history and exam. What else can help you?

4. How about ultrasound?

US is quick and reliable for the diagnosis of pneumonia.  US demonstrates a sensitivity of 95%, compared to 60% for CXR.33-35 US findings suggestive of pneumonia include air bronchograms, b-lines, consolidations, pleural line abnormalities, and pleural effusions. Pathognomonic findings include dynamic air bronchograms.33-35 Positive likelihood ratios (LR) for these findings are 15.6 to 16.8, with negative likelihood ratios of 0.03 to 0.07.33-35

Please see this video for more: https://www.youtube.com/watch?v=21yJm6IDuRA

You ultrasound the female patient, and on the left side you detect the following imaging:

Screen Shot 2017-03-03 at 8.58.29 PM

 You start antibiotics and fluids, as your suspicion on pneumonia has increased. What can you use to further characterize these findings?

5. How about CT?

Chest CT has a sensitivity that approaches 100%.19,30 In patients with suspected pneumonia, 27% have identifiable infiltrate on CT and nothing on CXR.30 Another study suggests CT reveals pulmonary infiltrates in 33% of patients with no finding on CXR, while excluding CAP in close to 30% of patients with infiltrates on CXR.19,28,30 CT is more precise and accurate for pneumonia.19,28,30  Like every test in the ED, the risks and benefits must be weighed, as CT has significant cost and increased radiation compared to CXR, and it can potentially increase the ED length of stay. It should not be used as the standard diagnostic tool.  However, in septic patients with no identifiable source and negative chest radiograph but upper respiratory symptoms suggestive of pneumonia, it should be considered.

CT chest noncontrast demonstrates infiltrate on the left. You continue your management.

 6. Ok, I’ve diagnosed pneumonia, and it seems to be community acquired. Who can go home? Are there scales or systems that can assist in making this decision?

There are a number of aspects that impact mortality from pneumonia. These are shown below.5,6,15,16,20,25

Finding Odds Ratio (95% CI)

Acute confusion

Shortness of breath

History of heart failure

History of cancer

History of neurologic disease

History of renal disease


2.0 (1.7-2.3)

2.9 (1.9-3.8)

2.4 (2.2-2.5)

2.7 (2.5-2.9)

4.4 (3.8-4.9)

2.7 (2.5-2.9)



Hypothermia (temperature < 37oC)

SBP < 100 mm Hg


2.5 (2.2-2.8)

2.6 (2.1-3.2)

5.4 (5.0-5.9)

Ancillary studies:

BUN > 20 mg/dL

WBC < 4 x 109 cells/L

WBC > 10 x 109 cells/L

Multilobar involvement


2.7 (2.3-2.0)

5.1 (3.8-6.4)

4.1 (3.5-4.8)

3.1 (1.9-5.1)

Scores or scales can assist in patient disposition by stratifying illness severity, including CURB-65 and PSI/PORT.5-7,25,31,32,45-48  CURB-65 was derived and validated in 2003. Based on this score, patients with 0 or 1 point can be discharged with antibiotic therapy. Patients with 2 points can be admitted or observed, while those with greater than 3 points should be admitted. Patients with score 4 or 5 should be admitted to the ICU.7,25,47,48 The CRB-65 scale may help when labs are difficult or not feasible, and CURB does not incorporate age.51,52 The table below shows the score, available on MDcalc: https://www.mdcalc.com/curb-65-score-pneumonia-severity

Predictor Score

BUN > 19 mg/dL (> 7 mmol/L)

Respiratory Rate > 30

Systolic BP < 90 mm Hg or Diastolic < 60 mm Hg

Age > 65 years











4 or 5

30-day Mortality:






The PSI/PORT score consists of a five-tier risk stratification system.7,25,31,32 It has been validated several times: one study of 38,000 admitted patients, and another study of 2,287 patients in an inpatient and outpatient setting.31,32,49-51 The score is based on age, comorbidities, physical exam, and labs, with completion requiring several steps.25,31,32,49,50,51 The first step entails evaluating patient age. Patients over 50 years are assigned to classes II – V.25,31,32,49-51 A diagram of the PSI/PORT score is shown below. This score can increase the number of patients treated as outpatient, with reduction in mortality and admission rates (by 15%).25,49-56 See MDCalc: https://www.mdcalc.com/psi-port-score-pneumonia-severity-index-cap. The SOAR score is another option, but we will not discuss this score here.25,46,57

Screen Shot 2017-03-03 at 8.58.52 PM

How do the scores compare?

Several studies have looked at score characteristics. PSI/PORT may have better sensitivity, with CURB-65 demonstrating greater specificity and PPV. Remember, PSI/PORT requires calculation with history, exam, labs, and CXR, while CURB-65 does not have hypoxemia or CXR findings. ROC curves are 0.81 for PSI, 0.73 for CURB, and 0.76 for CURB-65 in one study,50,51 with 0.736 for PSI and 0.694 for CURB-65 in another.58

Characteristic PSI

(95% CI)


(95% CI)


(95% CI)


(95% CI)

Pooled Sensitivity 0.90 (0.87-0.92) 0.62 (0.54-070) 0.63 (0.49-0.76) 0.33 (0.24-0.44)
Pooled Specificity 0.53 (0.46-0.59) 0.79 (0.75-0.83) 0.77 (0.68-0.83) 0.92 (0.86-0.96)
Positive Predictive Value 0.14 (0.13-0.16) 0.24 (0.19-0.30) 0.17 (0.14-0.22) 0.28 (0.18-0.41)
Negative Predictive Value 0.98 (0.98-0.99) 0.95 (0.93-0.97) 0.97 (0.96-0.97) 0.94 (0.92-0.95)
Diagnostic Odds Ratio 10.77 (8.29-13.97) 6.40 (5.05-8.10) 5.75 (4.59-7.21) 5.97 (3.41-10.44)

PSI/PORT can identify more patients as low risk. Keep in mind the scores may be better when used together to predict mortality, though this has not been evaluated. These scores do not assess social status. Homelessness, poor follow up, substance abuse, and PO intolerance are not accounted for in these scores, and they can underestimate severity in younger patients. Clinical gestalt is necessary in association with scores. 50,51,58-61

 The 24-year-old has a CURB-65 of 0 and PSI/PORT of 24 points (Class 1). The female has a CURB-65 of 2 and PSI/PORT 93 points (Class IV).

Bonus: What about biomarkers other than lactate?

A lot of research has focused on biomarkers. These include WBC, Procalcitonin (PCT), and CRP. Elevated WBC cannot be relied upon, with over ¼ of patients with confirmed pneumonia demonstrating normal WBC. 21,62-64  The +LR of 1.9-3.7 and poor specificity are also unreliable.16,20,25,51,60

PCT is released in response to bacterial infections, 65-68 with a meta-analysis finding a pooled sensitivity and specificity of 77% and 79%, respectively.66  Sensitivity for bacterial infection in another meta-analysis is 88%, with a specificity of 81%.67 Most studies to date have evaluated the use of PCT to determine when to discontinue antibiotics. However, studies including a Cochrane meta-analysis suggest PCT does not affect mortality, relapse rate, or length of stay.69-71

CRP comes from the liver in response to inflammation and possesses a sensitivity of 70% and specificity of 90% if a threshold of 40 mg/L is used for pneumonia diagnosis, though specificity is 65% in another study.72,73 

WBC, PCT, and CRP should not be used for routine evaluation of pneumonia, and further study is needed.

The 24-year-old male is looking better, now with normal VS. He wants to leave, and you discharge him with antibiotics. The female also feels improved following your resuscitation, but with her risk stratification score and your clinical gestalt, you discuss her case with the hospitalist, who agrees with you that she should be admitted.


– Pneumonia possesses a wide range of presentations.

– One study shows a prevalence of 2.6% for pneumonia in patients with URI symptoms, while other studies suggest this is closer to 7%.

No combination of history, exam, and testing can improve the diagnostic probability of pneumonia to over 50%.

– Patients younger than 65 years with normal vital signs and normal lung exam may not require a CXR. Patients with URI symptoms, vital sign abnormalities, and abnormal lung findings should have imaging.

– For imaging, US can be beneficial. Patients with high likelihood of pneumonia and negative CXR, such as those with immunosuppression, dehydration, and older age, may need additional imaging such as CT chest.

– Clinical scores can assist in risk stratification and disposition, but they should only be used in association with clinical judgment and gestalt.

Patient social situation, substance abuse history, and PO tolerance should be taken into consideration.


References/Further Reading:

  1. Halm EA, Teirstein AS. Management of community acquired pneumonia. N Engl J Med 2002;347:2039-45.
  2. Clinical Classifications for Health Policy Research: Hospital Inpatient Statistics, 1996. Rockville, MD, Agency for Health Care Policy and Research. HCPR publication no. 99-0034; 1999.
  3. National Vital Statistics Report: Deaths: Final Data for 2011. Vol 63, No. 3, 2013. http://www.cdc.gov/nchs/data/nvsr/nvsr63/nvsr63_03.pdf. Accessed October 07, 2016.
  4. gov – Hospital Compare. https://www.medicare.gov/hospitalcompare/search.html (Accessed on April 19, 2016).
  5. Kalil AC, Metersky ML, Klompas M, Muscedere J, Sweeney DA, Palmer LB, et al. Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clinical Infectious Diseases 2016;63(5):1-51.
  6. Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell GD, Dean NC, Dowell SF, File TM Jr, Musher DM, Niederman MS, Torres A, Whitney CG; Infectious Diseases Society of America; American Thoracic Society. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis. 2007 Mar 1;44 Suppl 2:S27-72.
  7. Wunderink RG, Waterer GW. Community-acquired pneumonia: pathophysiology and host factors with focus on possible new approaches to management of lower respiratory tract infections. Infect Dis Clin North Am 2004; 18:743.
  8. Strieter RM, Belperio JA, Keane MP. Host innate defenses in the lung: the role of cytokines. Curr Opin Infect Dis 2003; 16:193.
  9. Mason CM, Nelson S. Pulmonary host defenses and factors predisposing to lung infection. Clin Chest Med 2005; 26:11.
  10. Johansson N, Kalin M, Tiveljung-Lindell A, Giske CG, and Hedlung J. Etiology of community-acquired pneumonia:  Increased microbiological yield with new diagnostic methods.  Clin Infect Dis 2010; 50:202.
  11. Wunderink RG, Waterer GW. Community-acquired pneumonia. New Engl J Med 2014;370(6):543-51.
  12. de Roux A, Marcos MA, Garcia E, Mensa J, Ewig S, Lode H, Torres A. Viral community-acquired pneumonia in nonimmunocompromised adults.  Chest 2004; 125:1343.
  13. Chow AW, Benninger MS, Brook I, Brozek JL, Goldstein EJC, Hicks LA, et al. IDSA clinical practice guidelines for acute bacterial rhinosinusitis in children and adults. Clin Infect Dis 2012 Mar 20;
  14. Maloney G, Anderson E, Yealy DM. Chapter 65: Pneumonia and Pulmonary Infiltrates. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8th http://accessemergencymedicine.mhmedical.com/content.aspx?bookid=1658&sectionid=109429397. Accessed 03 October, 2016.
  15. Marrie TJ. Community-acquired pneumonia. Clin Infect Dis 1994; 18:501.
  16. Metlay JP, Kapoor WN, Fine MJ. Does this patient have community-acquired pneumonia? Diagnosing pneumonia by history and physical examination. JAMA 1997; 278:1440.
  17. Coley CM, Married TJ, Lave JR, et al. Processes and outcomes of care for patients with community-acquired pneumonia:  results from the Pneumonia Patient Outcomes Research Team (PORT) cohort study. Arch Intern Med 1999 May 10;159(9):970-80.
  18. Rosh AJ. Diagnosing pneumonia by medical history and physical examination. Ann Emerg Med 2005 Nov;46(5):465-467.
  19. Claessens YE, Debray MP, Tubach F, Brun AL, Rammaert B, Hausfater P, Naccache JM, Ray P, Choquet C, Carette MF, et al. Early chest computed tomography scan to assist diagnosis and guide treatment decision for suspected community-acquired pneumonia. Am J Respir Crit Care Med 2015;192:974–982.
  20. Metlay JP, Fine JM. Testing strategies in the initial management of patients with community-acquired pneumonia. Ann Intern Med. 2003;138:109-118.
  21. Marrie TJ. Community-acquired pneumonia in the elderly. Clin Infect Dis. 2000 Oct;31(4):1066-78.
  22. Riquelme R, Torres, A, el-Ebiary M, de la Bellacasa JP, Estruch R, Mensa J et al. Community-acquired pneumonia in the elderly:  A multivariate analysis of risk and prognostic factors.  Am J Respir Crit Care Med 1996 Nov;154(5):1450-5.
  23. Metlay JP, Schulz R, Li YH, Singer DE, Marrie TJ, Coley CM et al. Influence of age on symptoms at presentation in patients with community-acquired pneumonia.  Arch Intern Med 1997 Jul 14;157(13):1453-9.
  24. Fernandez-Sabe N, Carratala J, Roson B, Dorca J, Verdaguer R, Manresa F, Gudiol F. Community-acquired pneumonia in very elderly patients: causative organisms, clinical characteristics, and outcomes.  Medicine (Baltimore) 2003 May;82(3):159-69.
  25. Singanayagam A, Chalmers JD, Hill AT. Severity assessment in community-acquired pneumonia: a review. Q J Med 2009;102:379-88.
  26. Syrja H, Broas M, Suramo I, Ojala A, Lahde S. High-resolution computed tomography for the diagnosis of community-acquired pneumonia. Clin Infect Dis. 1998;27:358-63.
  27. Bartlett JG, Mundy LM. Community-acquired pneumonia. N Engl J Med. 1995;333:1618-24.
  28. Self WH, Courtney  DM, McNaughton  DC  et al. High discordance of chest x-ray and computed tomography for detection of pulmonary opacities in ED patients: implications for diagnosing pneumonia. Am J Emerg Med 2013;31:401-5.
  29. Hash RB, Stephens JL, Laurens MB, Vogel RL. The relationship between volume status, hydration, and radiographic findings in the diagnosis of community-acquired pneumonia. J Fam Pract. 2000;49:833-7.
  30. Hayden GE, Wrenn KW. Chest radiograph vs. computed tomography scan in the evaluation for pneumonia. J Emerg Med 2009 Apr;36(3):266-70.
  31. Fine MJ, Stone RA, Singer DE, Coley CM, Marrie TJ, Lave JR et al. Processes and outcomes of care for patients with community-acquired pneumonia: results from the Pneumonia Patient Outcomes Research Team (PORT) cohort study. Arch Intern Med 1999 May 10;159(9):970-80.
  32. Fine MJ, Auble TE, Yealy DM, Hanusa BH, Weissfeld LA, Singer DE, et al. A prediction rule to identify low-risk patients with community-acquired pneumonia. N Engl J Med 1997 Jan 23;336(4):243-50.
  33. Bourcier JE, Paquet J, Seinger M, Gallard E, Redonnet JP, Cheddadi F. Performance comparison of lung ultrasound and chest x-ray for the diagnosis of pneumonia in the ED. Am J Emerg Med. 2014 Feb;32(2):115-8.
  34. Hu QJ, Shen YC, Jia LQ, Guo SJ, Long HY, Pang CS, et al. Diagnostic performance of lung ultrasound in the diagnosis of pneumonia: a bivariate meta-analysis. Int J Clin Exp Med 2014 Jan 15;7(1):115-21.
  35. Chavez MA, Shams N, Ellington LE, Naithani N, Gilman RH, Steinhoff MC, et al. Lung ultrasound for the diagnosis of pneumonia in adults: a systematic review and meta-analysis Respir Res. 2014 Apr 23;15:50.
  36. Pauker SG, Kassirer JP. The threshold approach to clinical decision making. N Engl J Med. 1980;302:1109-17.
  37. Salkind AR, Cuddy PG, Foxworth JW. The rational clinical examination. Is this patient allergic to penicillin? An evidence-based analysis of the likelihood of penicillin allergy. JAMA. 2001;285:2498-505.
  38. Cohen ML. Epidemiology of drug resistance: implications for a post-antimicrobial era. Science. 1992;257:1050-5.
  39. Gonzales R, Bartlett JG, Besser RE, et al. Principles of appropriate antibiotic use for treatment of uncomplicated acute bronchitis: background. Ann Intern Med 2001; 134:521.
  40. Emerman CL, Dawson N, Speroff T, et al. Comparison of physician judgment and decision aids for ordering chest radiographs for pneumonia in outpatients. Ann Emerg Med 1991;20:1215.
  41. Graffelman AW, Cessie SL, Knuistingh Neven A, et al. Can history and exam alone reliably predict pneumonia? Fam Pract 2007;56:465.
  42. O’Brien WT, Rohweder DA, Lattin GE, et al. Clinical indicators of radiographic findings in patients with suspected community-acquired pneumonia: who needs a chest x-ray? J Am Coll Radiol 2006; 3: 703.
  43. Engle MF, Paling FP, Hoepelman AIM, van der Meer V, Oosterheert JJ. Evaluating the evidence for the implantation of C-reactive protein measurement in adult patients with suspected lower respiratory tract infection in primary care: a systematic review. Fam Pract 2012; 29: 383.
  44. Nolt BR, Gonzales R, Maselli J, et al. Vital-sign abnormalities as predictors of pneumonia in adults with acute cough illness. Am J Emerg Med 2007; 25: 631.
  45. Kamath A, Pasteur MC, Slade MG, et al. Recognising severe pneumonia with simple clinical and biochemical measurements. Clin Med 2003;3:54e6.
  46. Myint PK, Kamath AV, Vowler SL, Maisey DN, Harrison BD, British Thoracic Society. Severity assessment criteria recommended by the British Thoracic Society (BTS) for community-acquired pneumonia (CAP) and older patients. Should SOAR (systolic blood pressure, oxygenation, age and respiratory rate) criteria be used in older people? A compilation study of two prospective cohorts. Age Ageing 2006;35:286-91.
  47. Lim WS, van der Eerden MM, Laing R, et al. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax 2003;58:377-82.
  48. Lim WS, Lewis S, Macfarlane JT. Severity prediction rules in community acquired pneumonia: a validation study. Thorax 2000;55:219-23.
  49. Shah BA, Ahmed W, Dhobi GN, Shah NN, Khursheed SQ, Haq I. Validity of pneumonia severity index and CURB-65 severity scoring systems in community acquired pneumonia in an Indian setting. Indian J Chest Dis Allied Sci. 2010 Jan-Mar;52(1):9-17.
  50. Aujesky D, Auble TE, Yealy DM, Stone RA, Obrosky DS, Meehan TP, et al. Prospective comparison of three validated prediction rules for prognosis in community-acquired pneumonia. Am J Med. 2005 Apr;118(4):384-92.
  51. Loke YK, Kwok CS, Niruban A, Myint PK. Value of severity scales in predicting mortality from community-acquired pneumonia: systematic review and meta-analysis. Thorax 2010;65:884-890.
  52. Capelastegui A, España PP, Quintana JM, et al. Validation of a predictive rule for the management of community-acquired pneumonia. Eur Respir J. 2006;27(1):151-7.
  53. Yealy DM, Auble TE, Stone RA, Lave JR, Meehan TP, Graff LG, et al. Effect of increasing the intensity of implementing pneumonia guidelines: a randomized, controlled trial. Ann Intern Med. 2005 Dec 20;143(12):881-94.
  54. Renaud B, Coma E, Labarere J, Hayon J, Roy PM, Boureaux H. Routine use of the Pneumonia Severity Index for guiding the site-of-treatment decision of patients with pneumonia in the emergency department: a multicenter, prospective, observational, controlled cohort study. Clin Infect Dis. 2007 Jan 1;44(1):41-9.
  55. Carratalà J, Fernández-Sabé N, Ortega L, Castellsagué X, Rosón B, Dorca J, et al. Outpatient care compared with hospitalization for community-acquired pneumonia: a randomized trial in low-risk patients. Ann Intern Med. 2005 Feb 1;142(3):165-72.
  56. Atlas SJ, Benzer TI, Borowsky LH, et al. Safely increasing the proportion of patients with community-acquired pneumonia treated as outpatients. Arch Intern Med 1998;158:1350–6.
  57. Subramanian DN, Musonda P, Sankaran P, Tariq SM, Kamath AV, Myint PK. Performance of SOAR (systolic blood pressure, oxygenation, age and respiratory rate) scoring criteria in community-acquired pneumonia: a prospective multi-centre study. Age Ageing. 2013 Jan;42(1):94-7.
  58. Man SY, Lee N, Ip M, Antonio GE, Chau SS, Mak P, et al. Prospective comparison of three predictive rules for assessing severity of community-acquired pneumonia in Hong Kong. Thorax 2007;62:348-53.
  59. Ewig S, Kleinfeld T, Bauer T, Seifert K, Schäfer H, Göke N. Comparative validation of prognostic rules for community- acquired pneumonia in an elderly population. Eur Respir J 1999;14:370-5.
  60. Buising KL, Thursky KA, Black JF, MacGregor L, Street AC, Kennedy MP, et al. A prospective comparison of severity scores for identifying patients with severe community acquired pneumonia: reconsidering what is meant by severe pneumonia. Thorax 2006;61:419-24.
  61. Roson B, Carratala J, Dorca J, Casanova A, Manresa F, Gudiol F. Etiology, reasons for hospitalization, risk classes, and outcomes of community-acquired pneumonia in patients hospitalized on the basis of conventional admission criteria. Clin Infect Dis 2001;33:158-65.
  62. Furer V, Raveh D, Picard E, Goldberg S, Izbicki G. Absence of leukocytosis in bacteraemic pneumococcal pneumonia. Prim Care Respir J. 2011 Sep;20(3):276-81.
  63. Harper C, Newton P. Clinical aspects of pneumonia in the elderly veteran. J Am Geriatr Soc 1989;37:867-72.
  64. Gleckman R, Hibert O. Afebrile bacteremia. A phenomenon in geriatric patients. JAMA 1982;248:1478-82.
  65. Liu D, Su L, Guan W, Xiao K, Xie L. Prognostic value of procalcitonin in pneumonia: A systematic review and meta‐ Respirology (Carlton, Vic). 2016;21(2):280-288.
  66. Wacker C, Prkno A, Brunkhorst FM, Schlattmann P. Procalcitonin as a diagnostic marker for sepsis: a systematic review and meta-analysis. Lancet Infect Dis 2013 May;13(5):426-35.
  67. Simon L, Gauvin F, Amre DK, Saint-Louis P, Lacroix J. Serum procalcitonin and C-reactive protein levels as markers of bacterial infection: a systematic review and meta-analysis. Clin Infect Dis 2004 Jul 15;39(2):206-17.
  68. Maisel A, Neath S-X, Landsberg J, et al. Use of procalcitonin for the diagnosis of pneumonia in patients presenting with a chief complaint of dyspnoea: results from the BACH (Biomarkers in Acute Heart Failure) trial. European Journal of Heart Failure 2012;14(3):278-286.
  69. Bouadma L, Luyt CE, Tubach F, Cracco C, Alvarez A, Schwebel C, Schortgen F, et al. Use of procalcitonin to reduce patients’ exposure to antibiotics in intensive care units (PRORATA trial): a multicenter randomised controlled trial. Lancet 2010 Feb 6;375(9713):463-74.
  70. Jensen JU, Hein L, Lundgren B, Bestle MH, Mohr TT, Andersen MH, et al. Procalcitonin-guided interventions against infections to increase early appropriate antibiotics and improve survival in the intensive care unit: a randomized trial. Crit Care Med 2011 Sep;39(9):2048-58.
  71. Schuetz P, Müller B, Christ-Crain M, et al. Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections. Cochrane Database Syst Rev 2012;CD007498.
  72. Flanders SA, Stein J, Shochat G, et al. Performance of a bedside C-reactive protein test in the diagnosis of community-acquired pneumonia in adults with acute cough. Am J Med 2004; 116:529.
  73. Almirall J, Bolíbar I, Toran P, et al. Contribution of C-reactive protein to the diagnosis and assessment of severity of community-acquired pneumonia. Chest 2004; 125:1335.
  74. Diehr P, Wood RW, Bushyhead J, Krueger L, Wolcott B, Tompkins RK. Prediction of pneumonia in outpatients with acute cough—a statistical approach. J Chronic Dis 1984;37:215-25.
  75. Macfarlane J, Holmes W, Gard P, Macfarlane R, Rose D, Weston V, et al. Prospective study of the incidence, aetiology and outcome of adult lower respiratory tract illness in the community. Thorax 2001;56:109-14.

Medical Malpractice Insights: Learning from mistakes and dodging bullets

Author: Chuck Pilcher, MD, FACEP (Editor, Med Mal Insights) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

Thanks for allowing me to share excerpts from my free monthly opt-in email newsletter, Medical Malpractice Insights – Learning from Lawsuits. The goal of MMI-LFL is to improve patient safety, educate physicians, and reduce the cost and stress of medical malpractice lawsuits.

These posts will appear periodically on emDocs.net for reader enlightenment (and occasionally entertainment).

The first example below is from the September, 2016, issue which highlighted 3 cases of probable negligence that did not result in lawsuits – in the case below, only because the plaintiff (the deceased patient’s wife) died before the case could be filed. Being lucky is no substitute for being smart.

– Chuck Pilcher MD, FACEP, Editor, Med Mal Insights


Learning from mistakes and dodging bullets

When it’s CHF and not “walking pneumonia

Patient dies 20 hours after clinic visit for SOB and chest pain

Facts: An ARNP working in a rural Eastern Washington hospital clinic sees a 69 yo male diabetic, hyperlipidemic smoker who c/o SOB, chest tightness, and fatigue for the past 7 days. Other risk factors include peripheral vascular disease w/ fem-pop bypass, sleep screen-shot-2017-01-15-at-4-51-27-pmapnea, prior TIA, and CVA. He is on an ARB, ACE inhibitor, and Lipitor. Orthopnea is not documented. Exam shows a BP of 98/56 (low compared to prior clinic records) and HR 110 (high compared to prior clinic records.) No temperature is recorded. He also has a moist cough with scattered rhonchi but no wheezing. He is diagnosed with “walking pneumonia” and “SOB,” and is prescribed Augmentin and an Albuterol MDI. A brief differential listed does not include CHF. An x-ray done after leaving the clinic is reported as possible “early CHF.” The x-ray results are called to the patient by an MA and an appointment made for a F/U visit in 7 days. Twelve hours later the patient experiences a cardiac arrest. He is returned to the hospital via EMS and dies. Autopsy reveals coronary atherosclerosis and an MI “about 24 hours old.” An attorney is consulted by the surviving spouse.

Plaintiff: I had multiple risk factors for heart disease and an ACS, but you assumed my problem was related to my smoking. You didn’t address my chest tightness, low BP, or tachycardia. You didn’t even do an EKG because you didn’t consider CHF in your differential. You called it “pneumonia” yet didn’t even take my temperature. Besides, Augmentin is a poor choice for “walking pneumonia,” even if you were right. You didn’t even reconsider your diagnosis after you got the x-ray results, so why did you even bother to order one?

Defense: This case was reviewed prior to filing a lawsuit so no defense position is available.

Result: After review by two experts, the patient’s care was felt to be substandard for an ARNP or other primary care provider in a similar situation. A lawsuit was felt to have merit. However, the plaintiff (the surviving spouse) died before the case could be pursued and the attorney had no other reason to pursue it. A bullet was dodged.

Takeaway: Many steps were missed and assumptions made in this case. Keep an open mind in older patients with chest tightness and SOB.

  • Don’t anchor to one element of history, exemplified by the ARNP’s note that includes this: “As I walked into the room the air was impregnated with stale smoke.”
  • Review x-ray results with an open mind and be willing to reconsider your diagnosis.
  • Compare prior vital signs for significant changes.
  • Have a low threshold for getting an EKG in patients with “chest tightness.”
  • “Scattered rhonchi” are common in CHF.
  • Missing the diagnosis of “Walking pneumonia” is rarely life-threatening. Missing an acute coronary syndrome and/or new onset CHF can be rapidly fatal.
  • In the ED, there are a variety of pneumonia mimics: CHF, PE, aspiration, atelectasis, TB, septic emboli, foreign body, ARDS, and many others. The ED provider must consider and evaluate for these mimics. For more on this, please see this post: http://www.emdocs.net/pneumonia-mimics-pearls-and-pitfalls/





“We learn from failure, not from success.” Bram Stoker, Dracula

Must Know Antimicrobial Regimens – Adults

Authors: Marina N. Boushra, MD (EM Resident Physician, Vidant Medical Center) and Cassandra Bradby, MD (EM Attending Physician, Vidant Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

A 75-year-old man with a history of diabetes, hypertension, and dementia presents to the emergency department with a complaint of altered mental status. His nursing home caretaker endorses a dry cough for one week that has recently become productive and fevers with a Tmax of 38.9 ºC. She notes that he is not “acting like himself,” and elaborates that he is sleeping more, talking less, and has had multiple episodes of urinary incontinence, which is unusual for him. His vitals on arrival are T 38.5º C, HR 110, RR 30, BP 100/70. His exam is notable for somnolence, increased work of breathing with accessory muscle use, coarse rales at the base of the right lung, tachycardia, and dry mucus membranes.

Bacterial infections are a common diagnosis in the emergency department, and emergency physicians are often tasked with providing antibiotics for outpatient management or beginning antibiotics prior to admission. Antibiotic treatment is not without side effects, and treatment started in the emergency department is frequently empiric. Therefore, an understanding of the most likely causative organisms as well as local patterns of susceptibility and resistance is paramount to adequate treatment, appropriate antibiotic selection, and responsible antibiotic stewardship. Important historical details to elicit include allergies, recent antibiotic use, prior antibiotic failure, dialysis use, use of immunosuppressants or history of immunocompromise, culture results of prior infections, and contact with healthcare facilities, including recent hospitalization, living in a care facility, or recent invasive procedures such as ureteral catheterizations or intubation. These details offer vital information regarding possible bacterial resistance or the presence of opportunistic infection. Because multiple empiric regimens exist for infectious disease in the emergency department, contacting the hospital pharmacy about the local antibiogram may help tailor the empiric regimen to local microbial susceptibilities. Please keep this in mind with the recommendations discussed in each table. The following is a discussion of the most common or most emergent ED-diagnosed bacterial infections, their most likely causative organisms, and current recommendations for empiric treatment.


Pneumonia is infection of the pleural parenchyma and can be broadly divided into community-acquired (CAP) and hospital-acquired pneumonia (HAP). A third category of pneumonia, healthcare-associated pneumonia, is discussed in more detail later in this paper. The majority of pneumonia is community-acquired but historical details such as recent hospitalization, intubation, or ventilator dependence should raise concern for HAP and multi-drug resistant organisms (MDROs). Travel history may be important for more rare causes of pneumonia. In patients with known or suspected HIV or AIDS, pneumocystis pneumonia should be strongly considered.

Community-Acquired Pneumonia (CAP)

CAP can be caused by a variety of pathogens, with the most common bacterial cause being Streptococcus pneumonia1–3. Other common organisms include respiratory viruses, Haemophilus influenza, and Mycoplasma pneumoniae1–3. In patients requiring ICU admission, S. pneumoniae is still common, but there is increased prevalence of Legionella pneumophila, Staphylococcus aureus, gram-negative bacilli, and influenza4. It is important to remember these differences in etiology and to cover adequately for these serious organisms in patients requiring ICU admission. Patients with risk factors for aspiration pneumonia should receive additional anaerobic coverage. Treatment for CAP has become increasingly more complicated due to rising resistance to antibiotics. Risk factors for drug resistance include age >65, alcoholism, medical comorbidities, immunosuppressive illness or medication use, and use of beta-lactam, macrolide, or fluoroquinolone antibiotics in the last 3-6 months5,6.

Treatment should be initiated as soon as a diagnosis of CAP is made to prevent decompensation. CAP can often be treated on an outpatient basis. Studies have shown that physicians often use inconsistent criteria when making the decision to admit patients for the treatment of CAP and overestimate short-term patient mortality, leading to an increased rate of unnecessary hospitalizations7. The 2007 guidelines for the Infectious Disease Society of America (IDSA) and the American Thoracic Society (ATS) recommend using the CURB-65 score or Pneumonia Severity Index (PSI), both well validated prediction rules and decision aids, to aid in the risk stratification of patients and making the decision to admit for inpatient treatment7–9. Interestingly, a recent article investigating oral vs. intravenous fluoroquinolones for non-critically ill patients with CAP showed no difference in mortality, ICU transfers, or need for vasopressors or intubation10. Studies have shown shorter time to treatment and shorter hospital stays for patients started on oral rather than intravenous antibiotics11. As such, it is important to consider oral therapy in non-critically ill patients with CAP who are being admitted for treatment but are able to tolerate oral medication.

Studies have shown similar efficacy in CAP for fluoroquinolones and macrolides plus a penicillin or cephalosporin12. Importantly, there is a high rate of macrolide resistance in S. pneumoniae in the United States; as such, macrolides should not be used as empiric monotherapy in areas where resistance to macrolides is >25%5,13–15. Recommended regimens are outlined in the Table 1 below. The IDSA is expected to publish new guidelines for the treatment of CAP that better reflect current trends in resistance in the summer of 2017.

Hospital-Acquired (nosocomial) Pneumonia (HAP)

Pneumonia patients with recent hospitalizations present a challenge in antibiotic selection. While the pneumonia may be caused by an MDRO picked up in the healthcare environment, it is also possible that the patient has a simple community-acquired organism. The multi-drug resistant (MDR) score assesses a particular patient’s risk for infection with an MDRO16,17. Patients with a high MDR score should be presumed to have a pneumonia due to a resistant organism and treated accordingly with broad-spectrum coverage as outlined in Table 1 below. Patients with low MDR scores can be treated with the more narrow-spectrum coverage used for CAP, with the possibility of widening the spectrum in the event of treatment failure. The Shorr score is a similar scoring tool to assess the risk of infection by an MDR and tailor empiric coverage appropriately18.  Antibiotic treatment for presumed HAP should cover for Staphylococcus aureus and Pseudomonas aeruginosa19. Local antimicrobial prevalence and susceptibility, especially within the hospital, is helpful to determining a regimen, but can often be deferred to the judgement of the admitting team. Empiric regimens as recommended in the 2016 IDSA/ATS guidelines for empiric management of HAP are outlined in Table 1 below.

Healthcare-Associated Pneumonia (HCAP)

Healthcare-associated pneumonia (HCAP) refers to pneumonia that may have been acquired in healthcare facilities such as nursing homes and dialysis centers. It was formerly grouped with HAP due to presumed increased susceptibility to MDROs. Several studies, however, have shown no increased susceptibility to MDROs in patient with HCAP, and it is conspicuously missing from the IDSA/ATS guidelines on the management of HAP19–24. As such, in the absences of other historical susceptibilities to MDROs such as comorbidities or severe illness, patients with HCAP may be treated as CAP19–24.

Table 1: Empiric Treatment of Pneumonia based on type, setting, and patient-specific factors8,19

Type Setting Patient Factors Regimen
CAP Outpatient No recent antibiotics, co-morbidities, high-rate of resistance -Doxycycline 100mg bid for five days

-Azithromycin 500mg on day 1 followed by 250mg for four days.*

-Clarithromycin 500mg bid for seven days*

Recent antibiotics, co-morbidities, high-rate of resistance -Levofloxacin 750mg daily for five days

-Moxifloxacin 400mg daily for five days

-Gemifloxacin 320mg daily for five days

-Combination therapy with a beta-lactam (amoxicillin 1g tid, amoxicillin-clavulanate 2g bid, cefpodoxime 200mg bid, or cefuroxime 500mg bid) PLUS either a macrolide (azithromycin 500mg on day 1, followed by 250mg for four days, or clarithromycin 500mg bid for five days) or doxycycline 100mg bid for five days.

Inpatient Mild-Moderate disease, managed on general floor -Levofloxacin 750mg IV or po

-Moxifloxacin 400mg IV or po

-Combination therapy with a beta-lactam (cefotaxime 1-2g, ampicillin-sulbactam 1.5-3g, ceftriaxone 1-2g) PLUS a macrolide (azithromycin 500mg IV, or clarithromycin 500mg orally)

Severe disease requiring ICU admission -Combination therapy with a beta-lactam (cefotaxime 1-2g, ampicillin-sulbactam 1.5-3g, ceftriaxone 1-2g) PLUS a respiratory fluoroquinolone (levofloxacin 750mg IV, or moxifloxacin 400mg IV) OR azithromycin 500mg IV.

-If penicillin allergic, a respiratory fluoroquinolone PLUS aztreonam 1g

-If MRSA suspected, add vancomycin 15-20mg/kg IV

HAP Inpatient Combination therapy is warranted, with one from each of the following 3 categories:

1) Piperacillin-tazobactam 4.5 g IV, Cefepime 2 g IV, Ceftazidime 2g IV, Imipenem/cilastatin 500mg IV

2) Azithromycin 500mg IV, Ciprofloxacin 400mg IV, Levofloxacin 750mg IV, or Gentamicin 5-7mg/kg IV

3) Vancomycin 15-20mg/kg IV, Linezolid 600mg IV

*Macrolide antibiotics should not be used as empiric monotherapy in areas of known S. pneumoniae resistance >25% to macrolides. If such resistance exists, pair with a beta-lactam as shown in the table above.

Urinary Tract Infection

Urinary tract infections can involve the lower urinary tract (cystitis) or the upper tract (pyelonephritis). Urinary tract infections are very common in women, with sexually active women being at higher risk. Risk factors for urinary tract infections include recent sexual intercourse, prior urinary tract infections, and recent spermicide use25. When present in men, urinary tract infections are typically associated with underlying anatomical anomalies, recent catheterization, or other risk factors. While not all urinary tract infections in males are necessarily complicated, a search for these risk factors should be conducted when a male is diagnosed with a urinary tract infection.

Uncomplicated Cystitis

Urinary tract infections in women begin by bacterial colonization of the vagina by fecal bacteria, which may ascend via the urethra to infect the bladder and kidneys. Uncomplicated cystitis and pyelonephritis in women is typically caused by Escherichia coli, though Proteus mirabilis, Klebsiella pneumoniae, and Streptococcus saprophyticus are occasionally found26,27. Empiric treatment for uncomplicated urinary tract infections is best tailored to the regional E. coli sensitivities and is outlined in Table 328. Of note, this table may be modified based on local resistance patterns. Sterile pyuria should raise concern for a possible sexually-transmitted infection (STI) and patients who fail to improve despite appropriate antibiotic treatment should be tested for STI.

Complicated Urinary Tract Infection

A complicated urinary tract infection is one which is associated with a condition that increases the risk for therapeutic failure, as outlined in Table 2. The microbial spectrum of complicated UTI is more broad, including not only the typical organisms associated with uncomplicated UTI but also more varied and resistant pseudomonal, staphylococcal, and Serratia species as well as fungi29,30. Complicated lower urinary tract infections may be managed as an outpatient, but indications for hospitalization include inability to tolerate oral therapy or suspected/ documented infection with a resistant organism such as extended-spectrum beta-lactamase producing organisms (ESBLs). Complicated pyelonephritis is the progression of infection resulting in emphysematous pyelonephritis, corticomedullary or perinephric abscess, or papillary necrosis. Complicated pyelonephritis is an indication for admission and intravenous antibiotic treatment.

Table 2: Conditions that increase the risk of treatment failure in UTI (complicated UTI)

Renal failure
Hospital-acquired infection
Renal transplantation
Anatomic abnormality of the urinary tract
Symptoms >7 days prior to presentation
Presence of an indwelling foreign body (ureteral catheter, nephrostomy tube, ureteral stent)
Ureteral calculus

UTI and Asymptomatic Bacteriuria in the Pregnant Patient

Urinary tract infection and colonization in pregnant patients are worth special mention. While asymptomatic bacteriuria in a non-pregnant female does not warrant treatment, studies have shown a high rate of progression to symptomatic cystitis and pyelonephritis in pregnant patients31. As such, current recommendations suggest that any bacteriuria in a pregnant patient should be treated with antibiotics32. Additionally, although urinary tract infection in a pregnant woman is, by definition, complicated, fluoroquinolones, the first-line treatment for complicated cystitis, are a pregnancy class C medication and should be avoided33. Mild urinary tract infections in pregnant females are treated similarly to uncomplicated UTIs, as shown in Table 3 below. Follow-up cultures for resolution are important in this patient population34.

Table 3: Empiric treatment of uncomplicated and complicated urinary tract infections28,31,35.

Urinary Tract Infection Recommended regimen
Uncomplicated cystitis -Nitrofurantoin 100mg bid for five days*

-Trimethoprim-sulfamethoxazole 160/800mg bid for three days

-Cephalexin 500mg BID for 3-7 days

-Fosfomycin 3g in a single dose*

-Ciprofloxacin 250mg bid or Levofloxacin 250mg once per day for three days**

Complicated cystitis Outpatient:

-Ciprofloxacin 500mg bid or 1000mg daily for five to ten days

-Levofloxacin 750mg daily for five to ten days


-Levofloxacin 500mg IV

-Ceftriaxone 1g IV

-Ertapenem 1g IV

-Gentamicin 3-5mg/kg IV +/- ampicillin 1-2g every 4-6 hours***

-Tobramycin 3-5mg/kg IV +/- ampicillin 1-2g every 4-6 hours***

Uncomplicated Pyelonephritis




-Ciprofloxacin 500mg po bid for seven days or 1000mg daily for seven days

-Levofloxacin 750mg po daily for five to seven days


-Levofloxacin 500mg IV

-Ceftriaxone 1g IV

-Ertapenem 1g IV

-Gentamicin 3-5mg/kg IV

-Tobramycin 3-5mg/kg IV

Complicated Pyelonephritis – Inpatient, mild-moderate disease:

-Ceftriaxone 1g IV

-Ciprofloxacin 400mg IV

-Levofloxacin 750 mg IV

-Aztreonam 1g IV

Inpatient, severe disease:

-Cefepime 2g IV

-Ampicillin 1g IV four times per day plus Gentamicin 5mg/kg IV daily

-Piperacillin-tazobactam 3.375g IV

-Meropenem 500mg IV

-Imipenem 500mg IV

-Doripenem 500mg IV

Asymptomatic bacteriuria and acute cystitis in the pregnant patient -Nitrofurantoin 100mg po bid for five to seven days (in second or third trimester)*

-Trimethoprim-sulfamethoxazole 160/800 mg po bid for three days****

-Fosfomycin 3g po in a single dose*

-Amoxicillin-clavulanate 500mg po tid for three to seven days

-Cephalexin 500mg po bid for three to seven days

-Cefpodoxime 100mg po bid for three to seven days

*Fosfomycin and nitrofurantoin should be avoided if there is concern for early pyelonephritis.

**Fluoroquinolones, if possible, should be reserved for other important uses to avoid resistance against this class of antibiotics.

***Adding ampicillin provides Enterococcus coverage

****Should be avoided in first trimester and at term

Cellulitis and Soft-Tissue Infection

Cellulitis and Erysipelas

Cellulitis and erysipelas are bacterial skin infections that differ in that erysipelas involves the upper dermis and superficial lymphatics while cellulitis involves the deeper dermis and subcutaneous fat tissue. Both manifest with localized skin erythema, edema, warmth, and pain. Because of the more superficial nature of erysipelas, these lesions are typically more raised and better demarcated than cellulitis. Erysipelas also presents more acutely and with more systemic symptoms such as fevers and chills. The most common pathogens in cellulitis are beta-hemolytic streptococci and S. aureus, including methicillin-resistant S. aureus (MRSA)36–38. Beta-hemolytic streptococci are the most common cause of erysipelas36,39.

Lesions consistent with cellulitis should be examined closely for the presence of a drainable abscess. History is particularly important in the patient with possible cellulitis as cellulitis associated with human or animal bites or with water exposure needs different coverage than uncomplicated cellulitis. The presence of an indwelling device near the region of cellulitis is also important, as it is an indication of device infection.

The treatment of uncomplicated cellulitis is based on whether or not there is associated purulence. Current guidelines group erysipelas with non-purulent cellulitis in terms of treatment, as the lesions are often difficult to distinguish from each other and are caused by a similar spectrum of organisms. Patients with purulent cellulitis should receive empiric coverage for MRSA pending culture results40. Patients with non-purulent cellulitis or erysipelas should receive empiric coverage for beta-hemolytic streptococcus and MSSA, although patients with systemic symptoms, recurrent infection, or prior infection with MRSA should receive additional MRSA coverage36. Cellulitis can typically be managed as an outpatient; patients with signs of systemic toxicity, rapid progression, indwelling devices, or failure of outpatient management should be admitted for parenteral antibiotics. In addition to antibiotics, elevation of the affected area is an important aspect of treatment as it helps promotes drainage of edema and inflammatory substances, speeding symptomatic improvement36.

Table 4: Empiric treatment of cellulitis and erysipelas36

Infection Recommended regimen
Uncomplicated nonpurulent cellulitis without MRSA risk factors or erysipelas Outpatient -Dicloxacillin 500mg po qid for 5-10 days

-Cephalexin 500mg po qid for 5-10 days

-Clindamycin 450mg po tid for 5-10 days

Inpatient -Cefazolin 1-2g IV tid

-Ceftriaxone 1g IV every 24 hours

-Oxacillin or nafcillin IV every 4 hours

-Clindamycin 600-900mg IV tid

Uncomplicated purulent cellulitis or nonpurulent cellulitis with MRSA risk factors


Outpatient -Clindamycin 300-450mg po 3-4 times per day for 5-7 days

-Trimethoprim/sulfamethoxazole 1-2 DS tablets po bid for 5-7 days

-Doxycycline 100mg bid for 5-7 days

Inpatient -Vancomycin 15-20mg/kg/dose IV bid

-Clindamycin 600mg IV tid 

-Linezolid 600mg IV two times per day

-Daptomycin 4mg/kg/dose IV once daily

Skin abscesses

Skin abscesses are most commonly due to S. aureus (MRSA or MSSA), although polymicrobial infection with flora from the skin or adjacent mucosal tissues is also common36,40–42. Risk factors for MRSA infection include recent hospitalization or antibiotic use, contact with healthcare environments, institutionalization, HIV infection, intravenous drug use, and diabetes. Source control, in the form of warm compresses to promote drainage or incision and drainage, is important. The role of antibiotics following source control is debated. Studies have shown a slightly increased cure rate with the use of antibiotics following incision and drainage of uncomplicated abscesses, but also a higher rate of diarrhea and adverse effects43,44. Antibiotics should be started for large (>2cm) or multiple abscesses, extensive surrounding cellulitis, systemic symptoms, immunocompromise or co-morbidities, the presence of an indwelling device, or in cases where incision and drainage alone fails to achieve adequate clinical response36. Hospitalization and parenteral antibiotics should be considered for patients with extensive skin involvement or signs of systemic toxicity.

Table 5: Empiric antibiotic treatment of abscesses following source control36

Outpatient If suspicion for MRSA:

-Clindamycin 300-450mg po 3-4 times per day for 5-7 days

-Trimethoprim/sulfamethoxazole 1-2 DS tablets po bid for 5-7 days

-Doxycycline 100mg po bid for 5-7 days

If no suspicion for MRSA:

-Dicloxacillin 500mg po bid for 5-7 days

-Cephalexin 500mg po bid for 5-7 days

Inpatient -Vancomycin 15-20mg/kg/dose IV bid

-Clindamycin 600mg IV tid 

-Linezolid 600mg IV two times per day

-Daptomycin 4mg/kg/dose IV once daily

Sexually-Transmitted and Vulvovaginal Infections

Sexually transmitted infections (STI) are a diagnosis of immense public health importance. While the results of lab testing are often not available in the emergency department, physicians should have a low threshold for the initiation of treatment in patients with presentations consistent with STI. Treatment for common STIs is outlined in Table 6 below45. Counseling patients about safe sex practices and urging them to inform their partners is paramount to infection control.

Pelvic Inflammatory Disease

Pelvic inflammatory disease (PID) is infection of the upper genital tract (uterus, endometrium, fallopian tubes, ovaries) in women. PID may extend to involve adjacent structures, causing periappendicitis, pelvic peritonitis, and perihepatitis (Fitz-Hugh-Curtis syndrome). The majority of PID is caused by ascending sexually-transmitted infections (STI), with Neisseria gonorrhea and Chlamydia trachomatis being the most commonly implicated pathogens in PID45. The diagnosis of PID is often a presumptive one based on presentation. Due to the risk for tubal scarring leading to infertility or risk of ectopic pregnancy, even minimal symptoms without an alternative diagnosis warrant the start of antibiotic therapy to reduce the risk of serious complications due to delay of therapy. Mild to moderate disease can be treated as an outpatient. Indications for hospitalization and intravenous antibiotics include pregnancy, clinically severe disease, complicated PID (pelvic abscess), and intolerance to, noncompliance with, or failure of oral antibiotics. Empiric coverage for inpatient and outpatient management of pelvic inflammatory disease are outlined in Table 646,47.

Table 6: Recommended treatment regimens for select genitourinary infections45–47

Chlamydia -Azithromycin (1g po in one dose)

-Doxycycline (100mg bid for 7 day)

Gonorrhea* -Ceftriaxone (250mg IM or IV in one dose) plus azithromycin (1g po in one dose) or doxycycline (100mg bid for 7 days)
Trichomonas -Metronidazole (2g po in a single dose or 500mg bid for seven days)

-Tinidazole (2g po in a single dose)

Bacterial Vaginosis -Metronidazole (500mg  po bid for seven days)

-Metronidazole vaginal gel 0.75% (5g intravaginally for five days)

-Clindamycin vaginal gel 2% (5g intravaginally for seven days)

Candida Vulvovaginitis Fluconazole (150mg po in one dose)
Pelvic Inflammatory


Outpatient management -Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)

-Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)

Inpatient management -Ceftriaxone (250mg IM in one dose) plus doxycycline (100mg po bid for 14 days)

-Cefoxitin (2g IM) with probenecid (1g orally) plus doxycycline (100mg po bid for 14 days)

*Patients with gonorrhea should also be treated for chlamydia due to high rates of concomitant infection.

Bacterial meningitis

While meningitis is not as common an emergency department diagnosis as the bacterial infections discussed above, patients with meningitis are often quite ill, and knowledge of appropriate antibiotic coverage can speed time to therapy. The most common causes of community-acquired meningitis in adults in developed countries are Streptococcus pneumoniae, Neisseria meningitidis, and, in older adults, Listeria monocytogenes48,49. Empiric treatment should be initiated as soon as meningitis is suspected. Empiric regimens should include ceftriaxone (2g every 12 hours) or cefotaxime (2g every 4-6 hours) for coverage of N. meningitidis and S. pneumoniae as well as vancomycin due to increasing rates of S. pneumoniae resistance to third-generation cephalosporins50,51. In patients >50 years of age or with immunocompromise, ampicillin (2g every 4 hours) should be added to provide coverage for L. monocytogenes49.

Adverse Effects of Antibiotic Use

A discussion of antibiotic use in the emergency department would be remiss without mention of the adverse effects of antibiotics commonly used in the ED. While the use of certain antibiotics may be unavoidable due to patient allergies or susceptibility patters, knowledge of the adverse effects of antibiotics may help guide therapeutic choices and inform or temper patient expectations.

Clostridium difficile infection should always be a consideration when starting antibiotics. Clindamycin is the most common culprit in antibiotic-associated C. difficile infection, but cephalosporins, penicillins, and fluoroquinolones are also common causes52–56. Aminoglycosides, tetracyclines, metronidazole, and vancomycin are rarely associated with C. difficile infection, though any antibiotic use increases the risk for C. difficile infection57. Other important adverse effects include QT prolongation with arrhythmia associated with macrolide and fluoroquinolone use and the risk of peripheral neuropathy and (the uncommon, but oft-cited) tendon rupture with fluoroquinolone use. Common or serious side effects of antibiotics used in the emergency department are summarized in Table 7 below.

Table 7: Common and serious adverse effects of commonly used antibiotics

Antibiotic Common Adverse Effects Serious Adverse Effects Comments
Beta-lactams C. diff infection, diarrhea Hypersensitivity reactions High risk of C. diff, especially with broader coverage and with ampicillin
Macrolides Diarrhea, nausea, vomiting, abdominal pain QT prolongation (especially with erythromycin)
Clindamycin C. diff infection, diarrhea Serious hypersensitivity reactions Most common cause of C. diff
Fluoroquinolones Anorexia, nausea, vomiting, abdominal pain Tendon rupture, peripheral neuropathy, QT prolongation High C. diff risk
Tetracyclines Nausea, diarrhea, photosensitivity Inhibition of bone growth and tooth discoloration (a concern in children) Low C. diff risk
Vancomycin Abdominal pain, nausea Nephrotoxicity, ototoxicity, Red man syndrome, hypotension Red man syndrome can be prevented with pretreatment with antihistamines
Aminoglycosides Nephrotoxicity, ototoxicity Need frequent monitoring of drug levels
Metronidazole Headache, dizziness, metallic taste Disulfiram-like reaction Low C. diff risk
  • Summary

Table 8: Common and serious bacterial infections and recommended empiric treatment

Infection Important organisms to cover Recommended Regimens
Community-acquired pneumonia S. pneumoniae CAP outpatient: doxycycline, macrolide +/- penicillin or cephalosporin

CAP inpatient, mild: respiratory fluoroquinolone, macrolide + penicillin or cephalosporin

S. pneumoniae, L. pneumophila, S. aureus CAP inpatient, severe: penicillin or cephalosporin+ fluoroquinolone OR azithromycin
Hospital-acquired pneumonia S. pneumoniae, MRSA, P. aeruginosa HAP inpatient: anti-pseudomonal penicillin or cephalosporin, or fluoroquinolone, or carbapenem + vancomycin/linezolid
Uncomplicated cystitis E. coli Nitrofurantoin or fosfomycin or TMP/SMX or ciprofloxacin


Complicated cystitis or uncomplicated pyelonephritis E. coli, Pseudomonas sp., Staphylococcus sp. Outpatient: Fluoroquinolone

Inpatient: Fluoroquinolone or aminoglycoside or third-generation cephalosporin or carbapenem

Complicated pyelonephritis E. coli, Pseudomonas sp., Staphylococcus sp. Inpatient, mild-moderate: third-generation cephalosporin or monobactam

Inpatient, severe: anti-pseudomonal penicillin or cephalosporin, carbapenem

Asymptomatic bacteriuria or simple cystitis in the pregnant patient E. coli Nitrofurantoin or TMP/SMX or fosfomycin, or penicillin or cephalosporin with gram-negative coverage
Nonpurulent cellulitis or abscess without MRSA risk factors, erysipelas Beta-hemolytic streptococcal species, MSSA Outpatient and inpatient: staphylococcal penicillin or cephalosporin
Purulent cellulitis, nonpurulent cellulitis or abscess with MRSA risk factors Beta-hemolytic streptococcal species, MSSA, MRSA Outpatient: Clindamycin or TMP/SMX or doxycycline

Inpatient: Vancomycin or clindamycin

Chlamydia C. trachomatis Azithromycin or doxycycline
Gonorrhea N. gonorrhea AND C. trachomatis Ceftriaxone plus azithromycin or doxycycline
Trichomonas Trichomonas vaginalis Metronidazole or tinidazole
Bacterial vaginosis Polymicrobial, anaerobic gram-negative rods Metronidazole oral or intravaginal gel or clindamycin
Candida Vulvovaginitis C. albicans, C. glabrata Fluconazole
Pelvic Inflammatory Disease N. gonorrhea, C. trachomatis Inpatient and outpatient: third generation cephalosporin plus doxycycline
Bacterial meningitis S. pneumoniae, N. meningitidis, L. monocytogenes (if >50 years or immunocompromised) Vancomycin plus third generation cephalosporin +/- ampicillin if age >50 or immunocompromised


 References / Further Reading

  1. Johansson, N., Kalin, M., Tiveljung-Lindell, A., Giske, C. G. & Hedlund, J. Etiology of community-acquired pneumonia: increased microbiological yield with new diagnostic methods. Clin. Infect. Dis. 50, 202–9 (2010).
  2. Jain, S. et al. Community-Acquired Pneumonia Requiring Hospitalization among U.S. Adults. N. Engl. J. Med. 373, 415–27 (2015).
  3. Gadsby, N. J. et al. Comprehensive Molecular Testing for Respiratory Pathogens in Community-Acquired Pneumonia. Clin. Infect. Dis. 62, 817–23 (2016).
  4. Cillóniz, C. et al. Microbial aetiology of community-acquired pneumonia and its relation to severity. Thorax 66, 340–6 (2011).
  5. Vanderkooi, O. G. et al. Predicting antimicrobial resistance in invasive pneumococcal infections. Clin. Infect. Dis. 40, 1288–97 (2005).
  6. Ramsdell, J., Narsavage, G. L. & Fink, J. B. Management of Community-Acquired Pneumonia in the Home: An American College of Chest Physicians Clinical Position Statement. Chest 127, 1752–1763 (2005).
  7. Fine, M. J. et al. The hospital admission decision for patients with community-acquired pneumonia. Results from the pneumonia Patient Outcomes Research Team cohort study. Arch. Intern. Med. 157, 36–44 (1997).
  8. Mandell, L. A. et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin. Infect. Dis. 44 Suppl 2, S27-72 (2007).
  9. Lim, W. S. et al. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax 58, 377–82 (2003).
  10. Belforti, R. K. et al. Association Between Initial Route of Fluoroquinolone Administration and Outcomes in Patients Hospitalized for Community-acquired Pneumonia. Clin. Infect. Dis. 63, 1–9 (2016).
  11. Cyriac, J. M. & James, E. Switch over from intravenous to oral therapy: A concise overview. J. Pharmacol. Pharmacother. 5, 83–7 (2014).
  12. Ruhe, J. & Mildvan, D. Does Empirical Therapy with a Fluoroquinolone or the Combination of a β-Lactam Plus a Macrolide Result in Better Outcomes for Patients Admitted to the General Ward? Infect. Dis. Clin. North Am. 27, 115–132 (2013).
  13. Low, D. E. What Is the Relevance of Antimicrobial Resistance on the Outcome of Community-Acquired Pneumonia Caused by Streptococcus pneumoniae? (Should Macrolide Monotherapy Be Used for Mild Pneumonia?). Infect. Dis. Clin. North Am. 27, 87–97 (2013).
  14. Daneman, N., McGeer, A., Green, K., Low, D. E. & Toronto Invasive Bacterial Diseases Network. Macrolide resistance in bacteremic pneumococcal disease: implications for patient management. Clin. Infect. Dis. 43, 432–8 (2006).
  15. Jones, R. N., Sader, H. S., Moet, G. J. & Farrell, D. J. Declining antimicrobial susceptibility of Streptococcus pneumoniae in the United States: report from the SENTRY Antimicrobial Surveillance Program (1998-2009). Diagn. Microbiol. Infect. Dis. 68, 334–6 (2010).
  16. Park, S. C. et al. Validation of a scoring tool to predict drug-resistant pathogens in hospitalised pneumonia patients. Int. J. Tuberc. Lung Dis. 17, 704–709 (2013).
  17. Maruyama, T. et al. A new strategy for healthcare-associated pneumonia: a 2-year prospective multicenter cohort study using risk factors for multidrug-resistant pathogens to select initial empiric therapy. Clin. Infect. Dis. 57, 1373–83 (2013).
  18. Shorr, A. F. et al. A risk score for identifying methicillin-resistant Staphylococcus aureus in patients presenting to the hospital with pneumonia. BMC Infect. Dis. 13, 268 (2013).
  19. Kalil, A. C. et al. Management of Adults With Hospital-acquired and Ventilator-associated Pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin. Infect. Dis. 63, e61–e111 (2016).
  20. Chalmers, J. D., Rother, C., Salih, W. & Ewig, S. Healthcare-associated pneumonia does not accurately identify potentially resistant pathogens: a systematic review and meta-analysis. Clin. Infect. Dis. 58, 330–9 (2014).
  21. Ma, H. M., Wah, J. L. S. & Woo, J. Should nursing home-acquired pneumonia be treated as nosocomial pneumonia? J. Am. Med. Dir. Assoc. 13, 727–31 (2012).
  22. Yap, V., Datta, D. & Metersky, M. L. Is the present definition of health care-associated pneumonia the best way to define risk of infection with antibiotic-resistant pathogens? Infect. Dis. Clin. North Am. 27, 1–18 (2013).
  23. Ewig, S., Welte, T. & Torres, A. Is healthcare-associated pneumonia a distinct entity needing specific therapy? Curr. Opin. Infect. Dis. 25, 166–75 (2012).
  24. Kollef, M. H. Health care-associated pneumonia: perception versus reality. Clin. Infect. Dis. 49, 1875–7 (2009).
  25. Hooton, T. M. et al. A prospective study of risk factors for symptomatic urinary tract infection in young women. N. Engl. J. Med. 335, 468–74 (1996).
  26. Czaja, C. A., Scholes, D., Hooton, T. M. & Stamm, W. E. Population-based epidemiologic analysis of acute pyelonephritis. Clin. Infect. Dis. 45, 273–80 (2007).
  27. Echols, R. M., Tosiello, R. L., Haverstock, D. C. & Tice, A. D. Demographic, clinical, and treatment parameters influencing the outcome of acute cystitis. Clin. Infect. Dis. 29, 113–9 (1999).
  28. Gupta, K. et al. International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women: A 2010 update by the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases. Clin. Infect. Dis. 52, e103-20 (2011).
  29. Nicolle, L. E. Catheter-related urinary tract infection. Drugs Aging 22, 627–39 (2005).
  30. Nicolle, L. E. A practical guide to the management of complicated urinary tract infection. Drugs 53, 583–92 (1997).
  31. Smaill, F. M. & Vazquez, J. C. Antibiotics for asymptomatic bacteriuria in pregnancy. Cochrane database Syst. Rev. CD000490 (2015). doi:10.1002/14651858.CD000490.pub3
  32. Rouse, D. J., Andrews, W. W., Goldenberg, R. L. & Owen, J. Screening and treatment of asymptomatic bacteriuria of pregnancy to prevent pyelonephritis: a cost-effectiveness and cost-benefit analysis. Obstet. Gynecol. 86, 119–23 (1995).
  33. Hooper, D. C., Wolfson, J. S., Hooper, D. C. & Wolfson, J. S. Fluoroquinolone antimicrobial agents. N. Engl. J. Med. 324, 384–94 (1991).
  34. Patterson, T. F. & Andriole, V. T. Detection, significance, and therapy of bacteriuria in pregnancy. Update in the managed health care era. Infect. Dis. Clin. North Am. 11, 593–608 (1997).
  35. Stamm, W. E., Hooton, T. M. & Hooton, T. M. Management of urinary tract infections in adults. N. Engl. J. Med. 329, 1328–34 (1993).
  36. Stevens, D. L. et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clin. Infect. Dis. 59, (2014).
  37. Carratalà, J. et al. Factors associated with complications and mortality in adult patients hospitalized for infectious cellulitis. Eur. J. Clin. Microbiol. Infect. Dis. 22, 151–7 (2003).
  38. Siljander, T. et al. Acute bacterial, nonnecrotizing cellulitis in Finland: microbiological findings. Clin. Infect. Dis. 46, 855–61 (2008).
  39. Eriksson, B., Jorup-Rönström, C., Karkkonen, K., Sjöblom, A. C. & Holm, S. E. Erysipelas: clinical and bacteriologic spectrum and serological aspects. Clin. Infect. Dis. 23, 1091–8 (1996).
  40. Moran, G. J. et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N. Engl. J. Med. 355, 666–74 (2006).
  41. Singer, A. J. & Talan, D. A. Management of skin abscesses in the era of methicillin-resistant Staphylococcus aureus. N. Engl. J. Med. 370, 1039–47 (2014).
  42. Summanen, P. H. et al. Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use. Clin. Infect. Dis. 20 Suppl 2, S279-82 (1995).
  43. Talan, D. A. et al. Trimethoprim–Sulfamethoxazole versus Placebo for Uncomplicated Skin Abscess. N. Engl. J. Med. 374, 823–832 (2016).
  44. Schmitz, G. R. et al. Randomized Controlled Trial of Trimethoprim-Sulfamethoxazole for Uncomplicated Skin Abscesses in Patients at Risk for Community-Associated Methicillin-Resistant Staphylococcus aureus Infection. Ann. Emerg. Med. 56, 283–287 (2010).
  45. Workowski, K. A., Bolan, G. A. & Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines, 2015. MMWR. Recomm. reports Morb. Mortal. Wkly. report. Recomm. reports 64, 1–137 (2015).
  46. Ness, R. B. et al. Effectiveness of inpatient and outpatient treatment strategies for women with pelvic inflammatory disease: results from the Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) Randomized Trial. Am. J. Obstet. Gynecol. 186, 929–37 (2002).
  47. Walker, C. K. & Wiesenfeld, H. C. Antibiotic Therapy for Acute Pelvic Inflammatory Disease: The 2006 Centers for Disease Control and Prevention Sexually Transmitted Diseases Treatment Guidelines. Clin. Infect. Dis. 44, S111–S122 (2007).
  48. Schuchat, A. et al. Bacterial meningitis in the United States in 1995. Active Surveillance Team. N. Engl. J. Med. 337, 970–6 (1997).
  49. Clauss, H. E. & Lorber, B. Central nervous system infection with Listeria monocytogenes. Curr. Infect. Dis. Rep. 10, 300–6 (2008).
  50. Tunkel, A. R. et al. Practice guidelines for the management of bacterial meningitis. Clin. Infect. Dis. 39, 1267–84 (2004).
  51. Brouwer, M. C., Tunkel, A. R. & van de Beek, D. Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis. Clin. Microbiol. Rev. 23, 467–92 (2010).
  52. Pépin, J. et al. Emergence of fluoroquinolones as the predominant risk factor for Clostridium difficile-associated diarrhea: a cohort study during an epidemic in Quebec. Clin. Infect. Dis. 41, 1254–60 (2005).
  53. Deshpande, A. et al. Community-associated Clostridium difficile infection and antibiotics: a meta-analysis. J. Antimicrob. Chemother. 68, 1951–61 (2013).
  54. Johnson, S. et al. Epidemics of diarrhea caused by a clindamycin-resistant strain of Clostridium difficile in four hospitals. N. Engl. J. Med. 341, 1645–51 (1999).
  55. Tedesco, F. J., Barton, R. W. & Alpers, D. H. Clindamycin-associated colitis. A prospective study. Ann. Intern. Med. 81, 429–33 (1974).
  56. Gurwith, M. J., Rabin, H. R. & Love, K. Diarrhea associated with clindamycin and ampicillin therapy: preliminary results of a cooperative study. J. Infect. Dis. 135 Suppl, S104-10 (1977).
  57. Kelly, C. P., Pothoulakis, C. & LaMont, J. T. Clostridium difficile colitis. N. Engl. J. Med. 330, 257–62 (1994).


Pneumonia Mimics: Pearls and Pitfalls

Authors: Drew A. Long, BS (@drew2232, Vanderbilt University School of Medicine, US Army) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021, Senior Staff Physician, Henry Ford Hospital)

It’s a busy day in the ED. You have a full waiting room and multiple patients who have been roomed but not seen. You force your exhaustion to the back of your mind as you see your next patient: a 52-year-old male with cough and shortness of breath for three days. He states he has felt warm at home, but he denies chest pain, abdominal pain, vomiting, and diarrhea. He has experienced several episodes of nausea.  His past medical history includes hypertension and hyperlipidemia.

His vital signs include HR 103, RR 24, BP 128/72, T 99.8, and SpO2 95% on room air. He has some crackles in the lower lung bases, but has an otherwise normal physical exam. You order a chest x-ray, which demonstrates a right lower lobe infiltrate. As you write the diagnosis of “pneumonia” on the discharge form and write a prescription for antibiotics, you pause. Is there something else you could be missing? Are there other diagnoses you should consider?


Pneumonia is defined as an acute infection of the pulmonary alveoli.  Pneumonia can be life-threatening, most commonly in older patients with comorbidities or immunocompromised patients.  It is the 7th leading cause of death in the U.S. and the number one cause of death from infectious disease in the U.S.1   The annual incidence of community acquired pneumonia (CAP) ranges from 2 to 4 million, resulting in an estimated annual 500,000 hospitalizations.1  Pneumonia is broken into several categories: community-acquired (CAP), hospital-acquired, healthcare-associated (HCAP), and ventilator-associated (VAP) (Table 1).

Table 1.  Classification of Pneumonia (Adapted from Maloney G, Anderson E, Yealy DM.  Tintinalli’s Emergency Medicine:  A Comprehensive Study Guide.  Chapter 65:  Pneumonia and Pulmonary Infiltrates.  McGraw Hill Professional 2016.  8th ed.)



Community-acquired pneumonia



Acute pulmonary infection in a patient who is not hospitalized or residing in a long-term care facility 14 or more days before presentation



Hospital-acquired pneumonia


New infection occurring 48 hours or more after hospital admission




Healthcare-associated pneumonia


Patients hospitalized ≥ 2 days within past 90 days

Nursing home/long-term care residents

Patients receiving home IV therapy

Dialysis patients

Patients receiving chronic wound care

Patients receiving chemotherapy

Immunocompromised patients



Pneumonia can be caused by bacteria, viruses, or fungi.  However, it is often challenging to differentiate between these in the ED, and many patients will not have an etiologic agent identified even after inpatient evaluation.   It is estimated that a microbial agent cannot be identified in nearly half of cases of CAP.1 The “typical” pathogens in patients hospitalized with pneumonia include S. pneumoniae and H. influenza, with S. pneumoniae being the most common.  The “typical” pathogens are thought to account for about half of cases.1 “Atypical” pathogens include Legionella, Mycoplasma, and Chlamydia.  The most common identified viral causes of pneumonia are influenza and parainfluenza viruses.  Fungal pneumonia is often associated with patients who are immunocompromised or possess other risk factors.1,2

History and Physical Examination

The classic presentation of pneumonia is a cough productive of purulent sputum, shortness of breath, and fever.  The most common signs of pneumonia include cough (79%-91%), fever (up to 75%), increased sputum (up to 65%), pleuritic chest pain (up to 50%), and dyspnea (approximately 70%).3 There are many patterns of presentation with a variety of these symptoms and physical findings, making the diagnosis at times difficult. Elderly or debilitated patients in particular can present with non-specific complaints, such as altered mental status without the classic symptoms.1,2 In addition, pneumonia may cause lightheadedness, malaise, weakness, headache, nausea/vomiting, joint pain, and rash.  The examination may reveal bronchial or decreased breath sounds, dullness on percussion, rales, rhonchi, or wheezing. This wide variation in symptoms and presentation provides potential for misdiagnosis, especially if other conditions are not considered.

The chest x-ray in patients with pneumonia can vary greatly.  Radiologic findings in pneumonia are used in conjunction with the physical exam to identify any area of consolidation.  The most common cause of pneumonia, S. pneumoniae, classically presents with a lobar infiltrate visualized on chest x-ray.  Other organisms, such as Staphylococcus aureus pneumonia can be seen on chest x-ray as extensive infiltration and effusion or empyema.  Klebsiella may present with diffuse, patchy infiltrates.  Other findings on chest x-ray found in various organisms include pleural effusions, basilar infiltrates, interstitial infiltrates, or abscesses.1,2,4 However, each agent can present multiple ways on chest x-ray, and many patients may not demonstrate the classic radiographic findings, especially elderly and immunocompromised patients with weakened immune systems.

PA chest radiograph showing left upper lobe pneumonia.  (Image from Marx JA.  Rosen’s Emergency Medicine:  Concepts and Clinical Practice.  Saunders 2014.  8th ed.)

 While it is tempting to diagnose pneumonia in a patient with a classic presentation (fever, cough, shortness of breath) and a supportive chest x-ray, what else should be considered?  As Table 2 shows, many conditions can be confused for pneumonia based on the history, physical exam, and radiographic findings.

Table 2.  Mimics of Pneumonia (Adapted from Marx JA.  Rosen’s Emergency Medicine:  Concepts and Clinical Practice and Maloney G, Anderson E, Yealy DM.  Tintinalli’s Emergency Medicine:  A Comprehensive Study Guide.  Chapter 65:  Pneumonia and Pulmonary Infiltrates.)

Pulmonary Embolism
Septic Emboli
Congestive Heart Failure
Cancer and leukemic infiltrates
Acute Respiratory Distress Syndrome
Bronchiolitis obliterans organizing pneumonia
Granulomatous disease
Drug induced pulmonary disease
Pulmonary fibrosis
Eosinophilic pneumonia
Allergic/hypersensitivity pneumonitis
Radiation pneumonitis
Foreign body obstruction


Unfortunately, many of these diagnoses are not even considered in a patient with a classic presentation for pneumonia until the patient fails to improve with initial antibiotic management.  Of the diagnoses listed in Table 2, several of these carry high potential for morbidity and mortality.  These include pulmonary embolism, endocarditis, vasculitis, acute decompensated heart failure, tuberculosis, primary lung cancer, and acute respiratory distress syndrome.  The remainder of this discussion will focus on differentiating each of these from pneumonia.

*Bonus: What can potentially assist providers? Ultrasound (US)!

US has demonstrated tremendous utility differentiating pneumonia from other conditions. X-ray has a sensitivity of 46-77% in diagnosing pneumonia. US findings with pneumonia include air bronchograms, b-lines, consolidations, pleural line abnormalities, and pleural effusions. Dynamic air bronchograms (those that move) are considered pathognomonic for pneumonia.  Positive likelihood ratios (LR) for these findings range from 15.6 to 16.8, with negative LR’s of 0.03 to 0.07.5,6  Please see a prior emDocs.net post on the use of US in pneumonia: http://www.emdocs.net/ultrasound-for-pneumonia-in-the-ed/

Air bronchograms in pneumonia (From http://www.emdocs.net/ultrasound-for-pneumonia-in-the-ed/)

Pulmonary Embolism

Pulmonary embolism (PE) occurs when a thrombus, most commonly from the venous system, embolizes to the pulmonary vasculature.7,8 Like pneumonia, the clinical presentation of a PE can vary greatly, ranging from an asymptomatic patient to an ill-appearing, dyspneic patient.  PE can be easily confused with pneumonia, as the most common presenting symptom is dyspnea followed by pleuritic chest pain and cough.8,9 Fever can also be present in pulmonary embolism. The most common symptoms and their frequency are shown in Table 3.

Table 3.  Signs and Symptoms Of Pulmonary Embolism (adapted from Stein PD, Beemath A, Matta F, et al.  Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II. Am J Med. 2007;120(10):871.)

Sign/Symptom Frequency
Dyspnea 73%
Tachypnea 70%
Pleuritic Chest Pain 66%
Rales 51%
Cough 37%
Tachycardia 30%
S4 heart sound 24%
Accentuated P2 23%
Hemoptysis 13%
Circulatory collapse 8%


A PE most commonly has non-specific chest x-ray findings (atelectasis, pleural effusion, peripheral infarct/consolidation, elevated hemidiaphragm) or is normal.2  That being said, while a normal chest x-ray is helpful in distinguishing PE from pneumonia, a normal chest x-ray does not definitively exclude pneumonia or pulmonary embolism.  Hampton’s Hump (peripheral wedge-shaped opacity with base against pleural surface) and Westermark’s Sign (focus of oligemia and vessel collapse distal to the PE) are classic findings in the PE radiograph, but they lack sensitivity.

The important aspect of not missing PE is first considering it. As the presentation of PE is nonspecific, clinical gestalt and risk stratification are useful. Evaluate the patient for signs/symptoms of PE including shortness of breath with pleuritic chest pain, tachypnea, and leg swelling in the setting of risk factors such as recent travel history, prior history of thrombosis, family history of thrombosis, or history of cancer.  If signs and/or symptoms are present and concerning, do not hesitate to begin the workup for PE.

In PE, US may reveal RV strain with dilated RV and free wall hypokinesis and normal RV apical contractility (McConnell Sign). On short axis view, the LV will appear “D” shaped, with RV bowing into the LV due to elevated right-sided pressures.10-12

Enlarged RV when compared to LV in setting of acute PE (from www.em.emory.edu)


Endocarditis is most commonly caused by a bacterial agent, with a one-year mortality of 40%.13 The most common symptoms are intermittent fever (85%) and malaise (80%).1  Additionally, endocarditis can present with dyspnea, chest pain, cough, headache, weakness, and myalgias.  Infective endocarditis (IE) can easily be confused with pneumonia in a patient presenting with fever and dyspnea or chest pain.  Risk factors for IE are shown below in Table 4.  Diagnosis includes the Duke Criteria. A patient with flu-like symptoms (cough, myalgias, etc.) with the risk factors shown in Table 4, warrants further evaluation for IE. 13-17

Table 4.  Risk factors for IE

Age ≥ 60 (over half of cases occur in this population)
History of IV drug use
Poor dentition or dental infection
Structural heart disease (e.g. valvular or congenital)
Presence of prosthetic valve
Presence of intravascular device
Chronic hemodialysis


One of the most important aspects to not miss is the patient with multiple infiltrates on chest x-ray, as a dreaded complication of IE is septic emboli.  This has been described in 13 to 44% of patients with IE.18,19 Septic emboli can lead to damage in the systemic or pulmonary artery circulation, depending on left vs. right-sided disease.  Specifically, embolization can lead to stroke, paralysis, blindness, ischemia of the extremities, splenic or renal infarction, pulmonary emboli, or an acute myocardial infarction.18 In particular, septic emboli from the right heart to the pulmonary arteries can lead to a toxic-appearing patient with fever and shortness of breath.  Again, the chest x-ray may demonstrate multiple infarcts or consolidations. This patient may originally be worked up for pneumonia.  In the patient with IE risk factors described above and multiple consolidations/infarcts on chest x-ray, strongly consider IE and obtain multiple blood cultures and echocardiogram.  US may reveal valvular vegetation(s) and/or regurgitation.

Multiple emboli with consolidations from R sided IE (From https://www.roshreview.com/em.html)
Valvular Regurgitation with Vegetation in Endocarditis (From Journal of Medicine Cases, http://www.journalmc.org/index.php/JMC/article/view/286/212)

Vasculitis (Systemic Lupus Erythematosus)

A vasculitis that often manifests with pulmonary involvement is systemic lupus erythematosus (SLE).  SLE is an autoimmune disorder that leads to inflammation of multiple organ systems.  Pulmonary involvement is common and has been observed in up to 93% of patients with SLE.20,21 Lung involvement in SLE often manifests as pleurisy, coughing, and/or dyspnea.21-23 The most common respiratory condition among patients with SLE is pleuritis, thought to be due to autoantibodies damaging the pleura itself.1 Pneumonitis may also occur in the setting of SLE. Patients with acute lupus pneumonitis present with a rapid onset of fever, cough, and dyspnea, with elevation of serum antinuclear antibodies and anti-DNA antibodies.22,23

Patients with SLE (either diagnosed or undiagnosed) and lung involvement should be worked up for infection.  Since patients with SLE are often immunosuppressed due to immunomodulatory therapy and the disease itself, they are at a much higher risk of infection with both typical and opportunistic agents.  The patient with extrapulmonary features of SLE (e.g. malar rash, oral ulcers, polyserositis, renal insufficiency, cytopenia, thrombophilia, lymphadenopathy, splenomegaly, or arthritis) and signs of lung involvement warrants treatment for infection and worsening vasculitis. Consultation with rheumatology and the ICU is recommended due to the potential for rapid decompensation.

Diffuse alveolar hemorrhage (DAH) is one of the most life-threatening conditions in SLE. Diffuse alveolar damage is a more common presentation in patients who already have a documented history of lupus and rarely presents as the initial manifestation of lupus.  These patients present with severe shortness of breath, hemoptysis, and diffuse patchy infiltrates on chest x-ray. Patients often require intubation, ICU admission, and high dose steroids.24-26

Heart Failure Exacerbation

A patient with heart failure exacerbation can present similarly to a patient with pneumonia, particularly if a patient has undiagnosed heart failure.  Patients with acute decompensated heart failure most commonly present with cough, shortness of breath, fatigue, and/or peripheral edema.  The history and physical exam may be enough to differentiate a heart failure exacerbation from pneumonia.  A history of orthopnea and/or paroxysmal nocturnal dyspnea leading up to the patient’s presentation is sensitive and specific for heart failure.  Furthermore, many of these patients will have a cardiac history, history of cardiac procedures, and comorbid conditions for CHF (such as diabetes, hypertension, hyperlipidemia, or a history of smoking).  Physical exam may reveal an S3 or S4 heart sound, elevated jugular venous pressures, lower extremity edema, and crackles indicating interstitial pulmonary edema on auscultation of the lungs.  These patients often have nonspecific EKGs showing left-ventricular hypertrophy, bundle branch block, or signs of a previous MI such as prominent Q waves or T wave inversions.  BNP will more likely be elevated in CHF exacerbations, though sepsis from pneumonia can also increase BNP.1,27

The chest x-ray findings in CHF may include prominent interstitial markings, cardiomegaly, and pleural effusions.2

CXR in a patient with CHF depicting cardiomegaly, alveolar, and interstitial edema (From https://www.med-ed.virginia.edu/courses/rad/cxr/pathology2Bchest.html)

US in the setting of CHF will reveal b-lines in 3 or more lung fields bilaterally, which has a +LR of 20. The IVC will often reveal significant distension, with 2-2.5cm in size and < 50% collapse. Echocardiogram may reveal depressed contractility if systolic dysfunction is present.28

Multiple b-lines in the setting of acute CHF (From canadiem.org, http://canadiem.org/2015/01/19/us-world-ultrasound-differentiating-copd-chf/)


Tuberculosis (TB) is currently the world’s second leading infectious cause of death.1 The lungs are the major site for infection with Mycobacterium tuberculosis.  TB can occur in multiple forms, including primary TB, reactivation TB, laryngeal TB, endobronchial TB, lower lung field TB infection, and tuberculoma.29 As TB affects the lungs and can present with fever, cough, or dyspnea, it is often misdiagnosed as viral or bacteria pneumonia.  There are a wide array of nonspecific signs and symptoms associated with the multiple forms of TB, shown in Table 5.30

Table 5.  Symptoms and Signs of Tuberculosis (Adapted from Barnes PF, et al:  Chest roentgenogram in pulmonary TB: new data on an old test. Chest. 94:316, 1988.)

Symptom or Sign Frequency
Cough 78%
Weight loss 74%
Fatigue 68%
Tactile fever 60%
Night sweats 55%
Chills 51%
Anorexia 46%
Chest pain 40%
Dyspnea 37%
Hemoptysis 28%


In differentiating TB from pneumonia, it is important to assess the patient for risk factors for TB.  The most commonly reported behavioral risk factor among patients with TB in the U.S. is substance abuse (including drugs, tobacco, and alcohol).31 Other risk factors include malnutrition, systemic disease (silicosis, malignancy, diabetes, renal disease, celiac disease, or liver disease), or patients who are immunocompromised or homeless.32  Additionally, TB should be considered when a patient has a history of recent travel to an area where TB is endemic (Africa, the Middle East, Southeast and East Asia, and Central and South America).33

 As TB has many forms, the chest x-ray in TB can vary and may not be all that helpful in differentiating TB from pneumonia.  In summary, TB should be suspected in a patient with vague symptoms who possesses risk factors for TB, particularly in patients who are homeless, immunosuppressed, have a history of drug use, or have recently traveled to a TB endemic area.

Primary Lung cancer

In 2012, lung cancer worldwide was the most common cancer in men and the third most common cancer in women.34 In the U.S., lung cancer occurs in an estimated 225,000 patients every year and is responsible for over 160,000 deaths.35 There are many risk factors for cancer, the most notorious of which is smoking.

A patient with a primary lung cancer can easily be confused with pneumonia due to the similarity of symptoms (Table 6).  What is key in primary lung cancer is these symptoms have a more insidious onset than the relatively more acute onset of symptoms in pneumonia. Furthermore, these symptoms will progress over time and may include symptoms less commonly seen in pneumonia (weight loss, bone pain, or voice hoarseness).

Table 6.  Symptoms of lung cancer at presentation.  (Modified from: Hyde, L, Hyde, CI. Chest 1974; 65:299-306 and Chute CG, et al. Cancer 1985; 56:2107-2111).

Symptom Percent of Patients Affected
Cough 45-74%
Weight Loss 46-68%
Dyspnea 37-58%
Chest pain 27-49%
Hemoptysis 27-29%
Bone pain 20-21%
Hoarseness 8-18%


The chest x-ray in patients with lung cancer varies depending on the type and stage of cancer.  The chest x-ray in patients with a primary lung cancer may display a solitary nodule, an interstitial infiltrate, or may be normal.2

Non-small cell lung cancer.  (Image from http://emedicine.medscape.com/article/358433-overview)

 If considering a primary lung malignancy in a patient whose presentation is consistent with pneumonia, more definitive imaging including CT of the chest may be warranted. Discussion with the oncology service is advised.

Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome (ARDS) is acute, diffuse, inflammatory lung injury that carries high rates of morbidity, ranging from 26 to 58%.35,36 ARDS stems from diffuse alveolar damage and lung capillary endothelial injury, leading to increased capillary permeability and pulmonary edema.1 This disease manifests with respiratory distress, with patients often displaying tachycardia, tachypnea, hypoxemia, and dyspnea.37 Arterial blood gas analysis shows hypoxemia in addition to acute respiratory alkalosis and increased alveolar-arterial oxygen gradient (though ABG is usually not required in the ED).  A chest radiograph will typically reveal bilateral alveolar infiltrates, and classically, no cardiomegaly is seen.2

Chest radiograph depicting bilateral lung opacities in a patient with ARDS.  (Image from http://emedicine.medscape.com/article/362571-overview#a2)

When considering ARDS, several factors come into play.  The diagnosis of ARDS is complicated, as the most common cause or ARDS is sepsis. Thus, ARDS may result from a prior pneumonia leading to sepsis. The patient with ARDS will appear sick and will likely require high levels of FiO2 or positive pressure ventilation if not intubated, while the severity of pneumonia varies greatly based on the patient and infectious microbe.  Risk factors such as sepsis, aspiration, and multiple transfusions are commonly seen with ARDS.38 Other risk factors for ARDS include alcohol abuse, trauma, and smoke inhalation.  On physical exam, patients with ARDS often have diffuse crackles on auscultation of the lungs.  The chest x-ray shows more diffuse involvement than would be expected in a patient with pneumonia.2 US will reveal b-lines in multiple lung fields.  If concerned for ARDS, be ready to intubate the patient for clinical course/oxygenation and admit to the ICU.

Case resolution

As you return to this 52-year-old gentleman’s room with his prescription for antibiotics, you notice that he remains tachycardic, tachypneic, and hypoxic (HR 105, RR 24, SpO2 93%).  You perform a more complete review of systems and find out this gentleman has been experiencing pain in his right calf over the past week after returning from an overseas business trip.  On exam, you notice that his right lower extremity is slightly edematous compared to the left.  In addition to pneumonia, you decide to begin to work up this gentleman for a possible deep venous thrombosis and pulmonary embolism.  A chest CT reveals a large right-sided segmental PE.


Many potentially deadly conditions can be confused for pneumonia.  Unfortunately, many of these conditions are not considered until the patient fails to improve after treatment with antibiotics.  The following should be considered in a patient presenting with signs of pneumonia:

  • Pulmonary embolism: suspect when a patient has signs/symptoms of PE including shortness of breath with pleuritic chest pain, tachypnea, and leg swelling in the setting of risk factors for DVT/PE.
  • Endocarditis/septic emboli: consider in febrile patients with risk factors including history of IV drug use, poor dentition, structural heart disease, or the presence of a prosthetic valve. Septic emboli leading to pulmonary infarction can present with multiple infiltrates on chest x-ray.
  • Systemic Lupus Erythematosus: pulmonary involvement is very common in lupus. Patients with SLE and lung involvement must always be evaluated for infection, and diffuse alveolar hemorrhage is a life-threatening complication.
  • Heart Failure exacerbation: suspect in a patient with cardiac history and signs/symptoms of heart failure (orthopnea, PND, peripheral edema, elevated jugular venous distension, etc.).
  • Tuberculosis: suspect in patients with risk factors for TB including substance abuse, malnutrition, systemic diseases, immunocompromise, or recent foreign travel.
  • Lung cancer: suspect in patients with insidious onset of symptoms and in patients complaining of constitutional symptoms such as weight loss or fatigue.
  • Acute Respiratory Distress Syndrome: suspect in toxic-appearing patients with white-out on chest x-ray who require high levels of FiO2 or positive pressure ventilation.


References/Further Reading

  1. Marx JA. Rosen’s Emergency Medicine:  Concepts and Clinical Practice.  Saunders 2014.  8th
  2. Maloney G, Anderson E, Yealy DM. Tintinalli’s Emergency Medicine:  A Comprehensive Study Guide.  Chapter 65:  Pneumonia and Pulmonary Infiltrates.  McGraw Hill Professional 2016.   8th
  3. Fine MJ, Stone RA, Singer DE et al. Processes and outcomes of care for patients with community-acquired pneumonia:  results from the Pneumonia Patient Outcomes Research Team (PORT) cohort study.  Arch Intern Med 159:  970, 1999.
  4. Bartlett JG. Diagnostic approach to community-acquired pneumonia in adults.  UpToDate.  Jan 2016.
  5. Hu QJ, Shen YC, Jia LQ, et al. Diagnostic performance of lung ultrasound in the diagnosis of pneumonia: a bivariate meta-analysis. Int J Clin Exp Med. 2014;7(1):115-21. [pubmed]
  6. Chavez MA, Shams N, Ellington LE, et al. Lung ultrasound for the diagnosis of pneumonia in adults: a systematic review and meta-analysis. Respir Res. 2014;15:50. [pubmed]
  7. Thompson BT. Overview of acute pulmonary embolism in adults.  UpToDate.  Jan 2016.
  8. Thompson BT. Clinical presentation, evaluation, and diagnosis of the adult with suspected acute pulmonary embolism.  UpToDate.  Jan 2016.
  9. Stein PD, Beemath A, Matta F, et al. Clinical characteristics of patients with acute pulmonary embolism:  data from PIOPED II.  Am J Med.  2007;120(10):871.
  10. Perera, T. Mailhot, D. Riley, and D. Mandavia, “The RUSH exam: rapid ultrasound in Shock in the evaluation of the critically ill,” Emergency Medicine Clinics of North America, vol. 28, no. 1, pp. 29–56, 2010.
  11. P. Borloz, W. J. Frohna, C. A. Phillips, and M. S. Antonis, “Emergency department focused bedside echocardiography in massive pulmonary embolism,” Journal of Emergency Medicine, vol. 41, no. 6, pp. 658–660, 2011.
  12. Madan and C. Schwartz, “Echocardiographic visualization of acute pulmonary embolus and thrombolysis in the ED,” American Journal of Emergency Medicine, vol. 22, no. 4, pp. 294–300, 2004.
  13. Murdoch DR, Corey GR, Hoen B. Clinical Presentation, Etiology and Outcome of Infective Endocarditis in the 21st Century:  The International Collaboration on Endocarditis-Prospective Cohort Study.  Arch Intern Med.  2009 Mar 9;169(5):463-473.
  14. Sexton DJ. Epidemiology, risk factors, and microbiology of infective endocarditis.  UpToDate.  Jan 2016.
  15. Hill EE, Herijgers P, Claus P. Infective endocarditis:  changing epidemiology and predictors of 6-month mortality:  a prospective cohort study.  Eur Heart J.  2007;28(2):196.
  16. Cantrell M, Yoshikawa TT. Infective endocarditis in the aging patient.  Gerontology.  1984;30(5):316.
  17. Castillo FJ, Anguita M, Castillo JC, et al. Changes in the Clinical Profile, Epidemiology and Prognosis of Left-sided Native-valve Infective Endocarditis Without Predisposing Heart Conditions.  Rev Esp Cardiol (Engl Ed).  2015 May;68(5):445-8.  Epub 2015 Mar 16.
  18. Spelman D, Sexton DJ. Complications and outcome of infective endocarditis.  UpToDate.  Jan 2016.
  19. Steckelberg JM, Murphy JG, Ballard D, et al. Emboli in infective endocarditis:  the prognostic value of echocardiography.  Ann Intern Med.  1991;114(8):635.
  20. Dellaripa PF, Danoff Sonye. Pulmonary manifestations of systemic lupus erythematosus in adults.  UpToDate.  Jan 2016.
  21. King Jr. TE, Kim EJ, Kinder BW. Connective tissue diseases:  In:  Interstitial Lung Disease, 5th, Schwartz MI, King TE Jr. (Eds), People’s Medical Publishing House-USA, Shelton, CT 2011.
  22. Matthay RA, Schwarz MI, Petty TL, et al. Pulmonary manifestations of systemic lupus erythematosus:  review of twelve cases of acute lupus pneumonitis.  Medicine (Baltimore).  1975;54(5):397.
  23. Wiedemann HP, Matthay RA. Pulmonary manifestations of systemic lupus erythematosus.  J Thorac Imaging.  1992;7(2):1.
  24. Zamora MR, Warner ML, Tuder R, Schwarz MI. Diffuse alveolar hemorrhage and systemic lupus erythematosus.  Clinical presentation, histology, survival, and outcome.  Medicine (Baltimore).  1997;76(3):192. 
  25. Andrade C, Mendonca T, Farinha F, et al. Alveolar hemorrhage in systemic lupus erythematosus:  a cohort review.  Lupus.  2016 Jan;25(1):75-85.  Epub 2015 Sep 18.
  26. Collard HR, Schwarz MI. Diffuse alveolar hemorrhage. Clin Chest Med 2004;25:583–592, vii.
  27. Borlaug BA. Clinical manifestations and diagnosis of heart failure with preserved ejection fraction.  UpToDate.  Jan 2016.
  28. Ang S-H, Andrus P. Lung Ultrasound in the Management of Acute Decompensated Heart Failure. Current Cardiology Reviews. 2012;8(2):123-136.
  29. Pozniak A. Clinical manifestations and complications of pulmonary tuberculosis.  UpToDate.  Jan 2016.
  30. Barnes PF, et al: Chest roentgenogram in pulmonary TB:  new data on an old test.  94:316, 1988.
  31. Oeltmann JE, Kammerer JS, Pevzner ES, Moonan PK. Tuberculosis and substance abuse in the United States, 1997-2006.  Arch Intern Med.  2009;169(2):189.
  32. Horsburgh CR. Epidemiology of tuberculosis.  UpToDate.  Jan 2016.
  33. World Health Organization. Global Tuberculosis Report 2014. http://www.who.int.proxy.library.vanderbilt.edu/tb/publications/global_report/en/.
  34. World Cancer Research Fund International. Worldwide Data.  http://www.wcrf.org/int/cancer-facts-figures/worldwide-data.
  35. MacCallum NS, Evans TW. Epidemiology of acute lung injury.  Curr Opin Crit Care.  2005;11(1):43.
  36. Rubenfeld GD, Caldwell E, Peabody E, et al. Incidence and outcomes of acute lung injury.  N Engl J Med.  2005;353(16):1685.
  37. Hansen-Flaschen J, Siegel MD. Acute respiratory distress syndrome:  Clinical features and diagnosis in adults.  UpToDate.  Jan 2016.
  38. Siegel MD. Acute respiratory distress syndrome:  Epidemiology, pathophysiology, pathology, and etiology in adults.  UpToDate.  Jan 2016.

Ultrasound for Pneumonia in the ED

Ultrasound for Pneumonia in the ED

By Stephen Alerhand (@SAlerhand)
EM Resident Physician, Icahn School of Medicine at Mount Sinai

Edited by Alex Koyfman MD (@EMHighAK)

Patient Case

A 62 year-old obese male with a past medical history of diabetes and hypertension, is brought in by EMS at 3 AM complaining of subjective fever and weakness for 3 days. The patient appears fatigued, so his wife communicates on his behalf. He had been in is his usual state of health until demonstrating a marked decrease in energy 3 days ago of unclear origin. He denies cough, chest pain/palpitations, nausea/vomiting/diarrhea, or lower-extremity swelling. He denies recent travel, sick contacts, or a change in medications.

ED vitals: T 100.2, HR 80, BP 105/80, O2 sat 96% on room air.

Exam: Fatigued-appearing obese male, lung sounds unremarkable though diminished 2/2 body habitus, otherwise unremarkable.

Despite his overtly fatigued appearance, the patient’s vital signs do not meet SIRS criteria, and the nurses happen to triage him to one of the regular areas of the emergency department, where he will likely wait a little awhile before being seen by a resident.

Shortly thereafter, on her routine check of patients in the corner pocket of the ED, a nurse documents new vitals and presents them to the attending:

T 101.2, HR 90, BP 95/60, O2 sat 90% on room air

Along with his fatigued appearance (now critically assessed without the anchoring bias of ‘normal’ vital signs), the patient meets SIRS criteria and is transferred to the critical care/resuscitation area of the ED. Oxygen is administered, the patient is put on a monitor, and another peripheral IV line is obtained.

The resident suspects infection and considers pneumonia due to the fever and oxygen requirement. Unfortunately, the patient’s obesity contributes to suboptimal assessment. Specifically, lung sounds are again difficult to auscultate through the soft tissue, his weight makes him difficult to turn, and the STAT portable chest x-ray provides minimal diagnostic information.

Ultrasound Application

The resident grabs the ultrasound, sticks the probe on the patient’s right flank, and within 20 seconds reveals a lung consolidation to the rest of the team, promptly initiating antibiotic treatment specifically geared towards pneumonia. His attending physician, having practiced for 30 years in the community setting, cannot help but be impressed with his resident’s use of point-of-care ultrasound to diagnose pneumonia when “everybody knows that chest x-ray is the diagnostic imaging modality of choice.”

The Literature

Citation: Cortellaro, F. et al. Lung ultrasound is an accurate diagnostic tool for the diagnosis of pneumonia in the emergency department. Emerg Med J 2012;29:19-23.
Type of Study: Prospective (n=81)
Objective: To evaluate diagnostic accuracy of US
Results: US sensitivity 98%, specificity 85%. Exam always performed in < 5 min. CXR sensitivity 67%, specificity 85%.
Conclusion: US reliable for diagnosing PNA in ED, probably superior to CXR. Faster diagnosis. More timely therapy.

Citation: Parlamento, S. Copetti, R. di Bartolomeo, S. Evaluation of lung ultrasound for the diagnosis of pneumonia in the ED. Amer Journ EM 2009; 27:379-384.
Type of Study: Prospective (n=49)
Objective: Assess ability of US to confirm PNA and feasibility of integration into common ED practice
Results: US confirmed PNA in 32 of 49 (65.3%). In this group, 31 positive US (96.9% sensitivity), 24 positive CXR (75% sensitivity). Thus, 8 w/ positive US and negative CXR. Follow-up was consistent with diagnoses.
Conclusion: Bedside, reliable, rapid, noninvasive. Could have significant role in ED.

Citation: Reissig, A. Kroegel, C. Sonographic diagnosis and follow-up of pneumonia: a prospective study. Respiration 2007;74:537-547.
Type of Study: Prospective
Objective: To evaluate sonographic features of PNA at admission and during course of treatment
Results: Most characteristic feature of PNA was a positive bronchoaerogram. During follow-up, it decreased in size/number and disappeared quite often.
Conclusion: US well-suited for follow-up of PNA.

Citation: Chavez, M. Shams, N. Ellington, L. Lung ultrasound for the diagnosis of pneumonia in adults: a systematic review and meta-analysis. Respiratory Research 2014; 15:50.
Type of Study: Meta-analysis (n=1172)
Objective: Summarize existing evidence of diagnostic accuracy of US for PNA
Results: US took maximum of 13 min to conduct. Sensitivity and specificity of 94% and 96%, respectively.
Conclusion: US by highly-skilled sonographers performs well for diagnosing PNA.

Citation: Hu, J. et al. Diagnostic performance of lung ultrasound in the diagnosis of pneumonia: a bivariate meta-analysis. Int J Clin Med 2014;7(1):115-121.
Type of Study: Meta-analysis (n=1080)
Objective: To establish diagnostic accuracy of US for PNA
Results: Sensitivity 97%, specificity 94%, positive likelihood ratio 15.62, negative likelihood ratio 0.03.
Conclusion: High accuracy. Promising attractive alternative.

Tips/Tricks/Notes for Performing US to Evaluate for PNA

  • In pneumonia, alveoli accumulate with infectious contents. Sound waves travel through this matter as they would for soft tissue organs, such as the liver. The image on screen becomes solid and homogenous. Unsurprisingly, this concept is called “hepatization.”

liver vs consolidation

  • Low-frequency probe preferred for imaging of deep lung tissues
  • Within a consolidation, hyperechoic air bronchograms correspond to air in the bronchi. These air bubbles within the consolidation move with respiration, whereas the consolidation size does not change (unlike with a pleural effusion)


air bronchograms

  • Locate the diaphragm within the picture, as the liver and consolidation can appear similar.
  • Look along posterior axillary line in obese patients.


Advantages of Ultrasound versus X-ray

  • Real-time assessment of deterioration and/or response to treatment. Conversely, chest x-ray findings lag behind actual clinical lung exam.
  • Excellent for serial monitoring
  • Portable
  • Earlier diagnosis, earlier therapy
  • Less radiation
  • Cheaper
  • Better sensitivity/specificity as noted in several studies (see Literature above)
  • Distinguishes between lung consolidation and atelectasis
    • Air moving within bronchi will have bright and shimmery appearance of dynamic air bronchograms.
    • In contrast, for atelectasis, the air within the consolidation is static.
  • Also great for ICU care to follow dynamic lung changes for patients who can only get Portable films and not be transported for AP/Lateral films


Further References
–http://www.criticalecho.com/content/tutorial-9-lung-ultrasound (images)
–Introduction to Ultrasound, by Matt Dawson and Mike Mallin