Can pleural effusions be reliably detected using point-of-care ultrasound (POCUS)?

Absolutely. Though costophrenic blunting may not be seen on a PA or AP chest radiography until more than 200 mL of pleural effusion is present, as little as 20 mL of pleural fluid can be reliability detected with POCUS, with a sensitivity of 100% when more than 100 mL is present. Most pleural effusions will accumulate in the dependent areas within the chest cavity. Thus, in the usual semi-recumbent position used for POCUS, pleural effusion will accumulate above the diaphragm and below the lower lobe of the lungs.1,2

Few things to consider when evaluating for pleural effusion. 

  • Because evaluation for pleural effusions may require imaging depths of 10 to 20 cm, low frequency (preferably a phased array) transducer should be used.
  • Place the transducer in the posterior axillary line around the level of the diaphragm with the orientation marker positioned cephalad in the coronal plane (FIGURE 1).
  • Identify the diaphragm and use it as a point of reference to minimize mistakes such as labeling ascites as pleural effusion. Structures above the diaphragm (atelectatic lung, pleural effusion) will be shown on the left while structures below the diaphragm (abdominal organs, ascites) will be shown on the right side of the ultrasound display (FIGURE 2).
  • Keep in mind that freely flowing atelectatic lung tip (jellyfish sign) and spine shadows (spine sign) may be visible (VIDEO 1). Anechoic, free flowing pleural effusions are categorized as simple while homogeneously and heterogeneously echogenic effusions or those with septations are categorized as complex (VIDEO 2 and VIDEO 3). 2,3 
  • Smaller effusions may be seen as a small anechoic layer of fluid between the chest wall and the lung. If you use the M-mode, you will find that the lung moves towards or away from the chest wall in a wave like pattern (sinusoid sign) (VIDEO 4).1

Bonus Pearl: Did you know that you can estimate pleural effusion volume by using the following formula: Volume=16 x distance from mid lung base to the diaphragm (mm)? 4

Contributed by Woo Moon, D.O, Director, Hospitalist and Internal Medicine Residency Point-of-Care Ultrasound Programs, Mercy Hospital-St. Louis, St. Louis, Missouri

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     Figure 1                                                         Figure 2

Figure 3

Video 1

 

Video 2

 

Video 3

 

Video 4

 

References

  1. Soni NJ, Arntfield R, Kory P. Point of Care Ultrasound. 2nd ed. St. Louis, MO: Elsevier; 2019.
  2. Soni NJ, Franco R, Velez MI, et al. Ultrasound in the diagnosis and management of pleural effusions. J Hosp Med 2015;10(12):811–6. Ultrasound in the diagnosis and management of pleural effusions – PubMed (nih.gov) 
  3. Yang PC, Luh KT, Chang DB, Wu HD, et al. Value of sonography in determining the nature of pleural effusion: analysis of 320 cases. AJR Am J Roentgenol 1992;159(1):29–33.     Value of sonography in determining the nature of pleural effusion: analysis of 320 cases – PubMed (nih.gov)
  4. Usta E, Mustafi M, Ziemer G. Ultrasound estimation of volume of postoperative pleural effusion in cardiac surgery patients. Interact Cardiovasc Thorac Surg 2010;10(2):204–7. Ultrasound estimation of volume of postoperative pleural effusion in cardiac surgery patients – PubMed (nih.gov).

Disclosures/Disclaimers: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Can pleural effusions be reliably detected using point-of-care ultrasound (POCUS)?

Can I estimate the central venous pressure (CVP) of my patient with dyspnea at the bedside by using point of care ultrasound (POCUS)?

Absolutely! Not only can POCUS be used to estimate the CVP by measuring the jugular venous pressure (JVP), it may also be more reliable than the traditional—often challenging—visual method of looking for internal jugular (IJ) waveforms in the neck.1

To estimate the CVP by POCUS, first position the patient in a comfortable (usually semi-recumbent) position.   Select “vascular” (ie, high frequency) setting on your device (linear array probe for traditional ultrasound devices).  With the probe in the transverse plane (ie,  perpendicular to the IJ) and the orientation marker pointing to the right of the patient, slowly slide the probe cranially until the IJ appears to collapse during end-expiration, a point commonly referred to as the “meniscus” (CLIP 1 below). Measure the vertical distance between the meniscus and the sternal angle and, just as you would using the traditional method, add 5 cm (see limitation below) to calculate the height of the JVP, with values > 8 cm considered elevated (Figure 1 below).1,2,3

You can also look for the point of JVP collapse in the longitudinal axis by rotating the transducer 90° clockwise (CLIP 2 below).  Here, the shape of the IJ resembles a wine bottle with the collapsed portion or the tip of the tapered portion or triangle, representing the meniscus.3

A major limitation of estimating the CVP by visualization of JVP or by POCUS is the assumption that the distance between the right atrium and the sternal angle is constant at 5 cm.  It turns out that this distance may potentially vary among patients depending on their body habitus and position.4    A cool study from 2015, however, more accurately determined this distance by adjusted ultrasound views of the center of the right atrium. 5    Clearly, bedside estimation of CVP by POCUS will continue to be refined in the future. 

Bonus Pearl: Did you know that the traditional non-invasive method of estimating CVP by examining neck veins was first proposed in 1930 by Sir Thomas Lewis, a British cardiologist, who has been called the “father of clinical cardiac electrophysiology” and coined the terms “pacemaker,” “premature contractions,” and “auricular fibrillation”?6,7

 

Clip 1. Transverse visualization of the internal jugular vein (IJV) by using POCUS. The meniscus is the point of IJV collapse during end-expiration. 

 

Figure 1. Measurement of the jugular venous pressure (JVP) by POCUS. Add 5 cm (green arrow) to the distance between the meniscus (internal jugular collapse on the transverse view or tip of the tapering zone on the longitudinal view) and the sternal angle (red arrow).

Clip 2. Longitudinal visualization of the internal jugular vein (IJV) by using POCUS. The meniscus is the tip of the tapering zone or triangle of the IJV. 

 

 

 

Contributed by Woo Moon D.O., Mercy Hospital, St. Louis, Missouri

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References

1. Wang L, Harrison J, Dranow E, Aliyev N, Khor L. Accuracy of ultrasound jugular venous pressure height in predicting central venous congestion. Ann Intern Med 2021; 175:344-51.

2. McGee MD S. Evidence-Based Physical Diagnosis. 5th ed. Philadelphia: Elsevier; 2021.

3. Lipton B. Estimation of central venous pressure by ultrasound of the internal jugular vein. Am J Emerg Med 2000;18(4):432–4.

4. Istrail, L. POCUS and the jugular venous pressure: A deep dive. POCUS Med Ed, November 12. 2021. POCUS and the Jugular Venous Pressure: A Deep Dive (pocusmeded.com)

5. Xing C-Y, Liu Y-L, Zhao M-L, et al. New method for nonivasive quantification of central venous pressure by ultrasound. Circulation: Cardiovascular Imaging 2015;8/ https://doi.org/10.116/CIRCIMAGING.114.003085. New Method for Noninvasive Quantification of Central Venous Pressure by Ultrasound (ahajournals.org)

6. Sir Thomas Lewis – the Father of clinical cardiac electrophysiology | SciHi Blog [Internet]. [cited 2023 Feb 2]; Available from: http://scihi.org/thomas-lewis-cardiac-electrophysiology/

7. Lewis T. Remarks on early signs of cardiac failure of the congestive type. Br Med J 1930;1(3618):849–52.

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Can I estimate the central venous pressure (CVP) of my patient with dyspnea at the bedside by using point of care ultrasound (POCUS)?

“Should I consider cardiac CT angiography in my 76-year-old male patient with chest pain of unclear origin?”  

Probably not!1-4 Although the 2021 AHA/ACC Chest Pain Guidelines have generally widened the scope of indications for cardiac CT angiography (CCTA) to patients at low to intermediate risk of coronary artery disease (CAD) presenting with acute coronary syndrome (ACS)1 (with or without known CAD), several caveats should be considered before ordering this test. In general preference is given to patients with the following characteristics: 

  • Age sixty-five years of age or younger.  Elderly are not ideal candidates for CCTA as the calcium burden may be too high, rendering the test non-diagnostic due to the interference with proper coronary artery lumen assessment. Women tend not to accumulate as much calcium and their age threshold may be increased to 70 years. Some studies like the ROMICAT II Trial extended the age up to 74 years.4 
  • BMI <40.2
  • Sinus rhythm. Atrial fibrillation can be circumvented with expanded padding techniques, albeit at higher radiation exposure.2
  • Without coronary stents, unless their stents are > 3.0 mm in diameter (eg, in left main, very proximal left anterior descending, circumflex or right coronary stents).2
  • Without high coronary calcium burden, or without multiple risk factors for CAD (eg, type 2 diabetes, hypertension, hyperlipidemia) in the setting of typical anginal chest pain.1
  • Other technical requirements: must be able to hold breath during procedure, not have contraindications to beta blockers (ideal heart rate <60 bpm), not have an iodinated contrast allergy, and have stable kidney function.2

Despite these caveats, many patients may still be able to undergo CCTA to help exclude coronary causes of their chest pain.  For example, a 49-year-old patient at low to intermediate risk of CAD presenting with atypical chest pain can potentially undergo CCTA and, if negative, be discharged the same day!4  

In our patient, however, given his older age, CCTA is likely to be non-diagnostic and proceeding to an alternative test, such as stress test or invasive coronary angiography (depending on circumstances and pre-test probability), may be a better option.  

Bonus Pearl: Did you know that, as a “bonus”,  CCTA provides a “free” look at the lungs, calcium score (used largely in asymptomatic patients to help weigh pros and cons of starting a statin)3, and other cardiopulmonary structures that may hint at alternative diagnoses for the cause of chest discomfort and/or dyspnea?

Contributed by Eldin Duderija MD, Cardiologist, Mercy Clinic, St. Louis, Missouri

 

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References:

  1. Gulati M, Levy P, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain. J Am Coll Cardiol. 2021;78:e187–e285. https://pubmed.ncbi.nlm.nih.gov/34709879/
  2. Raff GL, Chinnaiyan KM, Cury RC, Garcia MT, Hecht HS, Hollander JE, O’Neil B, Taylor AJ, Hoffmann U; Society of Cardiovascular Computed Tomography Guidelines Committee. SCCT guidelines on the use of coronary computed tomographic angiography for patients presenting with acute chest pain to the emergency department: a report of the Society of Cardiovascular Computed Tomography Guidelines Committee. J Cardiovasc Comput Tomogr 2014;8:254-71. doi: 10.1016/j.jcct.2014.06.002. Epub 2014 Jun 12. PMID: 25151918. https://pubmed.ncbi.nlm.nih.gov/25151918/
  3. Hecht H, Blaha MJ, Berman DS, Nasir K, Budoff M, Leipsic J, Blankstein R, Narula J, Rumberger J, Shaw LJ. Clinical indications for coronary artery calcium scoring in asymptomatic patients: Expert consensus statement from the Society of Cardiovascular Computed Tomography. J Cardiovasc Comput Tomogr 2017;11:157-168. doi: 10.1016/j.jcct.2017.02.010. Epub 2017 Feb 24. PMID: 28283309. https://pubmed.ncbi.nlm.nih.gov/28283309/
  4. Hoffmann, Udo, et al. “Coronary CT angiography versus standard evaluation in acute chest pain.” N Engl J Med 2012;367:299-308. https://www.nejm.org/doi/full/10.1056/nejmoa1201161

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

“Should I consider cardiac CT angiography in my 76-year-old male patient with chest pain of unclear origin?”  

How do I assess the left ventricular (LV) systolic function by bedside point-of-care ultrasound (POCUS)?

You can assess the LV systolic function by POCUS by just zeroing in on the following cardiac parameters: 1. Anterior mitral valve leaflet motion in early diastole; 2. Change in LV chamber diameter; and 3. LV wall thickness during systole.1

First assess the anterior mitral valve leaflet motion towards the interventricular septum in early diastole in the parasternal long axis view (Figure). Estimated or measured distance between anterior mitral valve leaflet and the interventricular septum is called E-point septal separation (EPSS). When LV systolic function is normal, anterior mitral valve leaflet opens fully in early diastole, resulting in a small or minimal separation between it and the interventricular septum. Due to the fixed length of the chordae and the enlarged LV chamber size, anterior mitral valve leaflets are unable to fully open as systolic function worsens. This results in increased separation between the anterior mitral valve leaflet and the interventricular septum. An estimated EPSS greater than 10 mm is considered abnormal and suggests LV dysfunction.1,2

You can also estimate the LV ejection fraction (LVEF) quantitatively  by utilizing the following formula:3

LVEF (%)=75.5 – 2.5xEPSS (mm)

Keep in mind that aortic insufficiency and mitral stenosis can affect the accuracy of this formula.1

As for assessing the LV chamber diameter and wall thickness, recall that these parameters are also dynamic throughout the cardiac cycle. In systole, LV diameter should decrease by 30-40% while LV wall thickness should increase by approximately 40%. Using this as a guide, you can perform qualitative assessment by “eyeballing” the LV systolic function in parasternal long axis, parasternal short axis, apical 4-chamber and subcostal 4-chamber views. Beware that in parasternal long axis, apical 4-chamber and subcostal 4-chamber views, off axis of images can foreshorten the chamber size, resulting in overestimation of systolic function. Also be sure to use the midventricular papillary muscle view when assessing systolic function in the parasternal short axis.1   

Once you have obtained all the necessary images, feel free to categorize the systolic function as either “hyperdynamic”, “normal”, “reduced” or “severely reduced” (watch video below).1

Bonus pearl:  Did you know that qualitative assessment of the LV systolic function  following brief training sessions have been shown to significantly correlate with that obtained by formal echocardiography (k = 0.77, p <0.001).1,4,5 

Contributed by Woo Moon, D.O, Director POCUS Training Program, Mercy-St. Louis Hospital, St. Louis, Missouri

Figure: EPSS in normal vs reduced EF 

Note: EPSS (yellow arrows) is narrow in normal but wide in reduced EF

Video: Four categories of systolic function

 

References

  1. Soni MD MS NJ, Arntfield MD FRCPC R, Kory MD MPA P. Point of Care Ultrasound. 2nd ed. St. Louis, MO: Elsevier; 2019. . https://www.elsevier.com/books/point-of-care-ultrasound/soni/978-0-323-54470-2
  2. Kimura BJ, Yogo N, O’Connell CW, Phan JN, Showalter BK, Wolfson T. Cardiopulmonary limited ultrasound examination for “quick-look” bedside application. Am J Cardiol 2011;108(4):586–90. https://linkinghub.elsevier.com/retrieve/pii/S0002-9149(11)01424-X
  3. Silverstein JR, Laffely NH, Rifkin RD. Quantitative estimation of left ventricular ejection fraction from mitral valve E-point to septal separation and comparison to magnetic resonance imaging. Am J Cardiol 2006;97(1):137–40. https://www.ajconline.org/article/S0002-9149(05)01683-8/fulltext
  4. Melamed R, Sprenkle MD, Ulstad VK, Herzog CA, Leatherman JW. Assessment of left ventricular function by intensivists using hand-held echocardiography. Chest 2009;135(6):1416–20. https://journal.chestnet.org/article/S0012-3692(09)60341-X/fulltext 
  5. Johnson BK, Tierney DM, Rosborough TK, Harris KM, Newell MC. Internal medicine point-of-care ultrasound assessment of left ventricular function correlates with formal echocardiography. J Clin Ultrasound 2016;44(2):92–9. https://onlinelibrary.wiley.com/doi/10.1002/jcu.22272

 

 

 

 

 

 

 

How do I assess the left ventricular (LV) systolic function by bedside point-of-care ultrasound (POCUS)?

Is lung ultrasound useful in evaluating patients with dyspnea?

Yes! Increasingly, lung ultrasound (particularly point-of-care ultrasound-POCUS) is performed at bedside to help explain the cause of dyspnea.  Here are some tips.

First, obtain images by placing the transducer in the intercostal space (usually 3 regions/hemithorax) with the orientation marker pointing cephalad. 1,2  Now look at the pleural line, the horizontal hyperechoic structure between 2 ribs  (Figure 1). To and fro movement of the pleural line reflects apposition of the visceral and parietal pleura and is a normal finding (“lung sliding”).  Then look for additional horizontal hyperechoic lines visualized deep to the pleural line (“A-lines”) which are reverberation artifacts, reflecting air below the pleura (Clip/Figure 1).2 

You should also look for vertical laser like hyperechoic artifacts that arise from the pleural line and extend to the bottom of the display which may represent  “comet tails” or “B-lines” (Clip/Figure 2).1,3,4 These are reverberation artifacts created by the acoustic impedance difference between widened, fluid filled septa and air-filled alveoli.3,5  Three or more B-lines within a single intercostal space is considered pathological.4

One of the practical uses of lung ultrasound is in the evaluation of dyspnea in a patient with Chronic Obstructive Pulmonary Disease (COPD).6 The presence of lung sliding and bilateral A-lines in the absence of B-lines can help rule out pneumothorax, pneumonia and pulmonary edema and steer you toward other diagnoses (eg, COPD exacerbation) as cause of dyspnea.

You can even take it a step further. Focal unilateral B-lines suggest possible pneumonia while diffuse bilateral B-lines (interstitial syndrome) would be more consistent with pulmonary edema.

As usual, the patient’s history, physical examination and available laboratory data must be taken into consideration when interpreting lung ultrasound findings.2,4

Contributed by Woo Moon, D.O., Department of Medicine, Mercy-St. Louis, St. Louis, Missouri

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Figure 1 

 

 

Clip 1

 

 

Figure 2

 

Clip 2

 

References

  1. Lichtenstein DA. Lung ultrasound in the critically ill. Ann Intensive Care 2014;4(1): https://pubmed.ncbi.nlm.nih.gov/24401163/&nbsp;
  2. Soni MD MS NJ, Arntfield MD FRCPC R, Kory MD MPA P. Point of Care Ultrasound. 2nd ed. St. Louis, MO: Elsevier; 2019.
  3. Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest 2008;134(1):117–25. https://pubmed.ncbi.nlm.nih.gov/18403664/&nbsp;
  4. Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Med 2012;38(4):577–91. https://pubmed.ncbi.nlm.nih.gov/22392031/&nbsp;
  5. Lichtenstein D, Mézière G, Biderman P, Gepner A, Barré O. The comet-tail artifact. An ultrasound sign of alveolar-interstitial syndrome. Am J Respir Crit Care Med 1997;156(5):1640–6. https://pubmed.ncbi.nlm.nih.gov/9372688/
  6. Qaseem A, Etxeandia-Ikobaltzeta I, Mustafa RA, et al. Appropriate Use of Point-of-Care Ultrasonography in Patients With Acute Dyspnea in Emergency Department or Inpatient Settings: A Clinical Guideline From the American College of Physicians. Ann Intern Med 2021;174(7):985–93. https://www.acpjournals.org/doi/10.7326/m20-7844&nbsp;

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis, Massachusetts General Hospital, Harvard Catalyst, Harvard University, their affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Is lung ultrasound useful in evaluating patients with dyspnea?

Can race affect the accuracy of pulse oximetry measurement?

It can! In persons with darkly pigmented skin, pulse oximeters may overestimate arterial oxygen saturation, such that some individuals with oxygen saturation within an acceptable range by pulse oximetry may actually be hypoxemic by arterial blood measurement.1-3

A 2020 study involving 2 large patient populations with oxygen saturations of 92-96% by pulse oximetry, found occult hypoxemia (<88% arterial oxygen saturation) in ~12% of patients who were Black vs ~4% of those who were White. Black individuals were 3 times more likely to have occult hypoxemia than White patients.1

Overestimation of oxygen saturation—particularly at low arterial oxygen saturation— by pulse oximetry in dark-skinned individuals has been previously reported by several studies, although some have not found significant differences at normal saturations, and the degree of discordance may vary among various pulse oximeters.2,3

The reason for the apparent discrepancy between oxygen saturation measured by pulse oximetry vs arterial blood sample in those with dark skin is unclear. Some have suggested “pulse oximeter optical factors” and theorized that provision of correction factors, tables, or even built-in user -optional adjustments may be necessary.2

Given the frequent use of pulse oximetry for medical decision making in Covid-19, these studies should serve as a cautionary note when interpreting oxygen saturation by pulse oximeter in dark-skinned patients with Covid-19.

Bonus Pearl: Did you know that falsely-LOW oxygen saturation has been reported with blue and green nail polish but not red?4

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References

  1. Sjoding MW, Dickson RP, Valley TS. Racial bias in pulse oximetry measurement. N Engl J Med 2020;383:2477-78. https://pubmed.ncbi.nlm.nih.gov/33326721/
  2. Bickler PE, Feiner JR, Severinghaus JW. Effects of skin pigmentation on pulse oximeter accuracy at low saturation. Anesthesiology 2005;102:715-9. https://pubs.asahq.org/anesthesiology/article/102/4/715/7364/Effects-of-Skin-Pigmentation-on-Pulse-Oximeter
  3. Zeballos RJ, Weisman. Reliability of noninvasive oximetry in Black subjects during exercise and hypoxia. Am Rev Resp Dis 1991;144:1240-4. https://www.atsjournals.org/doi/pdf/10.1164/ajrccm/144.6.1240
  4. Cote CJ, Goldstein EA, Fuchsman WH. The effect of nail polish on pulse oximetry. Anesth Analg 1988;75:683-6. https://pubmed.ncbi.nlm.nih.gov/3382042/

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Can race affect the accuracy of pulse oximetry measurement?

How long should I expect Legionella urine antigen test to remain positive after diagnosis of legionnaire’s disease in my patient with pneumonia?

The urine antigen test for detection of Legionnaire’s disease (LD) can remain positive for weeks or months after initial infection. So a positive test in a patient with pneumonia may not just be suggestive of an acute infection but also the diagnosis of LD during recent weeks or months (1,2).

In a study of Legionella urine antigen detection as a function of days after onset of symptoms, 11 of 11 (100%) patients tested remained positive after day 14 (1). In the same study, 10 of 23 (43%) patients excreted antigen for 42 days or longer following initiation of therapy, with some patients remaining positive for more than 200 days!

In another study involving 61 patients with Legionella pneumophila pneumonia, 25% excreted Legionella antigen for 60 or more days (2). Longer duration of antigen excretion was significantly associated with immunosuppressed patients in whom the time to resolution of fever was > 72 h.

The long duration of excretion of Legionella antigen in urine following LD is not surprising. Pneumococcal pneumonia has also been associated with prolonged antigen excretion, some for as long as 6 months after diagnosis of pneumonia (3). It is thought that some microbial polysaccharides may be degraded very slowly or not at all by mammalian tissues which could explain their prolonged appearance in the urine long after active infection has resolved (1).

Bonus pearl: Did you know that the sensitivity of Legionella urinary antigen for LD varies from 94% for travel-associated infections to 76%-87% for community-acquired infection, and to as low as ~45% for nosocomially-acquired infections (4)?

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References

  1. Kohler RB, Winn WC, Wheat J. Onset and duration of urinary antigen excretion in Legionnaires disease. J Clin Microbiol 1984;20:605-7. https://pubmed.ncbi.nlm.nih.gov/6490846/
  2. Sopena N, Sabria M, Pedro-Bolet ML, et al. Factors related to persistence of Legionella urinary antigen excretion in patients with legionnaire’s disease. Eur J Clin Microbiol Infect Dis 2002;21:845-48. https://europepmc.org/article/med/12525918
  3. Andreo F, Prat C, Ruiz-Manzano J, et al. Persistence of Streptococcus pneumoniae urinary antigen excretion after pneumococcal pneumonia. Eur J Clin Microbiol Infect Dis 2009;28:197-201. https://pubmed.ncbi.nlm.nih.gov/18830727/
  4. Helbig JH, Uldum SA, Bernander S, et al. Clinical utility of urinary antigen detection for diagnosis of community-acquired, travel-associated, and nosocomial Legionnaire’s disease. Clin Microbiol 2003;41:838-40. https://pubmed.ncbi.nlm.nih.gov/12574296/

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

How long should I expect Legionella urine antigen test to remain positive after diagnosis of legionnaire’s disease in my patient with pneumonia?

What is the utility of nasal screen for methicillin-resistant Staphylococcus aureus (MRSA) in patients with skin and soft tissue infections?

In patients at high risk of MRSA infection (eg, prior history of MRSA colonization or infection, recent hospitalization/antibiotics, intravenous drug use, traumatic injury),1 particularly in the presence of an open wound or purulent drainage, a negative MRSA nasal screen does not rule out MRSA skin and soft tissue infection (SSTI), nor does a positive MRSA nasal screen reliably predict MRSA SSTI. In contrast, in low risk patients without severe disease, a negative MRSA nasal screen may be helpful in deescalating empiric anti-MRSA coverage.

The sensitivity of MRSA nasal screen by culture or PCR for SSTIs may be as low as 40%, higher among those with an ulcer (70%), with negative predictive values of 80% to 98% depending on the prevalence of MRSA in the population; its specificity is better (72% to 96%) with positive predictive values of 7% to 76%. 2

In a retrospective study involving 57 diabetic patients hospitalized with foot wound infection, the sensitivity of MRSA nasal screen was only ~40% with a negative predictive value of 80%. 3 Another study found a negative predictive value of ~90% for MRSA nasal screen among patients with a diabetic foot infection when MRSA isolation from wounds was uncommon (7.5%).4

Several reasons explain why patients with a negative MRSA nasal screen could still have MRSA SSTI, including colonization in other body sites known to harbor MRSA (eg, rectum, axilla, groin, oropharynx) 6-9 or direct wound contamination with MRSA in the absence of carriage, particularly in healthcare facilities.10

Bonus Pearl: Did you know that dogs, particularly those owned by healthcare workers, may also carry MRSA in their nostrils?.11,12

 

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References

  1. Stevens DL, Bisno AL, Chambers H, et al. Practice guidelines for the diagnosis and treatment of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis 2014; 59:e10-52. https://www.idsociety.org/practice-guideline/skin-and-soft-tissue-infections/
  2. Carr AL, Daley MJ, Merkel KG, et al. Clinical utility of methicillin-resistant Staphylococcus aureus nasal screening for antimicrobial stewardship: A review of current literature. Pharmacotherapy 2018;38:1216-1228. https://accpjournals.onlinelibrary.wiley.com/doi/abs/10.1002/phar.2188
  3. Lavery LA, La Fonatine J, Bhavan K, et al. Risk factors for methicillin-resistant Staphylococcus aureus in diabetic foot infections. Diabet Foot Ankle 2014;5:10.3402/dfa.v5.23575. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3984406/
  4. Mergenhagen KA, Croix M, Starr KE, et al. Utility of methicillin-resistant Staphylococcus aureus nares screening for patients with a diabetic foot infection. Antimicrob Agents Chemother 2020;64:e02213-19. https://pubmed.ncbi.nlm.nih.gov/31988097/  
  5. Currie A, Davis L, Odrobina E, et al. Sensitivities of nasal and rectal swabs for detection of methicillin-resistant Staphylococcus aureus colonization in an active surveillance program. J Clin Microbiol 2008;46:3101-3103. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2546770/
  6. Mermel LA, Cartony JM, Covington P, et al. Methicillin-resistant Staphylococcus aureus colonization at different body sites: a prospective, quantitative analysis. J Clin Microbiol 2011;49:1119-21. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3067701/#B4
  7. Baker SE, Brecher SM, Robillar E, et al. Extranasal methicillin-resistant Staphylococcus aureus colonization at admission to an acute care Veterans Affairs Hospital. Infect Control Hosp Epidemiol 2010;31:42-6. https://pubmed.ncbi.nlm.nih.gov/19954335/
  8. Manian FA, Senkel D, Zack J et al. Routine screening for methicillin-resistant Staphylococcus aureus among patients newly admitted to an acute rehabilitation unit. Infect Control Hosp Epidemiol 2002;23:516-9. https://pubmed.ncbi.nlm.nih.gov/12269449/
  9. Lautenbach E, Nachamkin I, Hu B, et al. Surveillance culture for detection of methicillin-resistant Staphylococcus aureus: diagnostic yield of anatomic sites and comparison of provider- and patient-collected samples. Infect Control Hosp Epidemiol 2009;30:380-82. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665909/
  10. Boyce JM, Bynoe-Potter G, Chenevert C, et al. Environmental contamination due to methicillin-resistant Staphylococcus aureus: possible infection control implications 1997;18:622-7. https://pubmed.ncbi.nlm.nih.gov/9309433/  
  11. Boost MV, O’donaghue MM, James A. Prevalence of Staphylococcus aureus among dogs and their owners. Epidemiol Infect 2008;136:953-64. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2870875/#ref017
  12. Manian FA. Asymptomatic carriage of mupirocin-resistant methicillin-resistant Staphylococcus aureus (MRSA) in a pet dog associated with MRSA infection in household contacts. Clin Infect Dis 2003;36;e26-28. https://academic.oup.com/cid/article/36/2/e26/317343

 

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What is the utility of nasal screen for methicillin-resistant Staphylococcus aureus (MRSA) in patients with skin and soft tissue infections?

How might categorizing severity of illness help in the management of my patient with Covid-19?

Although the criteria for Covid-19 severity of illness categories may overlap at times or vary across guidelines and clinical trials, I have found those published in the National Institute of Health (USA) Covid-19 Treatment Guidelines most useful and uptodate.1  Keep in mind that the primary basis for severity categories in Covid-19 is the degree by which it alters pulmonary anatomy and physiology and respiratory function (see my table below).

The first question to ask when dealing with Covid-19 patients is whether they have any signs or symptoms that can be attributed to the disease (eg, fever, cough, sore throat, malaise, headache, muscle pain, lack of sense of smell). In the absence of any attributable symptoms, your patient falls into “Asymptomatic” or “Presymptomatic” category.  These patients should be monitored for any new signs or symptoms of Covid-19 and should not require additional laboratory testing or treatment.

If symptoms of Covid-19 are present (see above), the next question to ask is whether the patient has any shortness of breath or abnormal chest imaging. If neither is present, the illness can be classified as “Mild” with no specific laboratory tests or treatment indicated in otherwise healthy patients. These patients may be safely managed in ambulatory settings or at home through telemedicine or remote visits. Those with risk factors for severe disease (eg, older age, obesity, cancer, immunocompromised state), 2 however, should be closely monitored as rapid clinical deterioration may occur.

Once lower respiratory tract disease based on clinical assessment or imaging develops, the illness is no longer considered mild. This is a good time to check a spot 02 on room air and if it’s 94% or greater at sea level, the illness qualifies for “Moderate” severity. In addition to close monitoring for signs of progression, treatment for possible bacterial pneumonia or sepsis should be considered when suspected. Corticosteroids are not recommended here and there are insufficient data to recommend either for or against the use of remdesivir in patients with mild/moderate Covid-19.

Once spot 02 on room air drops below 94%, Covid-19 illness is considered “Severe”; other parameters include respiratory rate >30, Pa02/Fi02 < 300 mmHg or lung infiltrates >50%. Here, patients require further evaluation, including pulmonary imaging, ECG, CBC with differential and a metabolic profile, including liver and renal function tests. C-reactive protein (CRP), D-dimer and ferritin are also often obtained for their prognostic value. These patients need close monitoring, preferably in a facility with airborne infection isolation rooms.  In addition to treatment of bacterial pneumonia or sepsis when suspected, consideration should also be given to treatment with corticosteroids. Remdesivir is recommended for patients who require supplemental oxygen but whether it’s effective in those with more severe hypoxemia (eg, those who require oxygen through a high-flow device, noninvasive or invasive mechanical ventilation or extracorporeal membrane oxygenation-ECMO) is unclear. Prone ventilation may be helpful here in patients with refractory hypoxemia as long as it is not used to avoid intubation in those who otherwise require mechanical ventilation.

“Critical” illness category is the severest forms of Covid-19 and includes acute respiratory distress syndrome (ARDS), septic shock, cardiac dysfunction and cytokine storm. In addition to treatment for possible bacterial pneumonia or sepsis when suspected, corticosteroids and supportive treatment for hemodynamic instability and ARDS, including prone ventilation, are often required. The effectiveness of remdesivir in patients with severe hypoxemia (see above) is unclear at this time.

 

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 References

  1. NIH COVID-19 Treatment Guidelines. https://www.covid19treatmentguidelines.nih.gov/. Accessed Aug 27, 2020.
  2. CDC. Covid-19.  https://www.cdc.gov/coronavirus/2019-ncov/need-extra-precautions/people-with-medical-conditions.html/. Accessed Aug 27, 2020.  

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

How might categorizing severity of illness help in the management of my patient with Covid-19?

Could my patient with acute dysuria and less than 10,000 E. coli/ml on urine culture still have a urinary tract infection (UTI)?

Absolutely! Although historically ≥100,000 bacteria/ml has been used as a criterion for UTI based on studies of women with pyelonephritis in the 1950s,1 several studies have since found that this criterion may not be met in up to 50% of symptomatic patients with UTI. 2-6 A lower criterion of 100-1,000 bacteria/ml of urine increases the sensitivity of urine culture to ~90% or more for diagnosis of UTI (albeit with lower specificity). 2-5

A 1982 NEJM study involving UTIs due to coliforms in acutely dysuric women found that the traditional count of ≥100,000 bacteria/ml in midstream urine missed ~50% of cases based on positive bladder cultures. 2 Similarly a 2013 NEJM study reported that 40% of women with symptomatic UTI would be missed if the ≥100,000 bacteria/ml criterion for midstream urine is used. 3

Among symptomatic men, 32% have been found to have <100,000 bacteria/ml in their midstream urine 4 and a single urine specimen by urethral catheterization growing ≥ 100 bacteria/ml is consistent with bacteriuria for both men and women. 5

Since most of these studies have involved UTI caused by E. coli or other coliforms, more data are needed to find out if the same findings apply to non-coliform urinary pathogens.

Bonus Pearl: Did you know that because quantitative urine culture results are concentration dependent (ie, “per ml”), a dilute urine—as may be found in patients experiencing diuresis—will result in lower numbers of bacteria/ ml. 5

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 References

  1. Kass EH. Asymptomatic infections of the urinary tract. Trans Assoc Am Physicians 1958;69:56-74. https://pubmed.ncbi.nlm.nih.gov/13380946/
  2. Stamm WE, Counts GW, Running KR, et al. Diagnosis of coliform infection in acutely dysuric women. N Engl J Med 1982;307:463-8. https://pubmed.ncbi.nlm.nih.gov/7099208/
  3. Hooten TM, Roberts PL, Cox ME, et al. Voided midstream urine culture and acute cystitis in premenopausal women. N Engl J Med 2013;369:1883-91. https://www.nejm.org/doi/full/10.1056/NEJMoa1302186
  4. Lipsky BA, Ireton RC, Fihn SD, et al. Diagnosis of bacteriuria in men: specimen collection and culture interpretation. J Infect Dis 1987;155:847-54. https://pubmed.ncbi.nlm.nih.gov/3559288/
  5. Nicolle LE, Bradley S, Colgan R, et al. Infectious Diseases Society of America Guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults. Clin Infect Dis 2005;40:643-54. https://pubmed.ncbi.nlm.nih.gov/15714408/
  6. Roberts KB, Wald ER. The diagnosis of UTI: colony count criteria revisited. Pediatrics 2018;141:e20173239. https://doi.org/10.1542/peds.2017-3239

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

Could my patient with acute dysuria and less than 10,000 E. coli/ml on urine culture still have a urinary tract infection (UTI)?