Pulmonary edema;

Chest CT scan of my patient with congestive heart failure (CHF) and shortness of breath shows mediastinal adenopathy.  Can mediastinal adenopathy be caused by CHF alone?

FA Manian MD, MPH, , , , , , Leave a comment

Yes! Mediastinal adenopathy (commonly defined as 1 or more lymph nodes with a short axis diameter >1 cm) may be caused by CHF alone (AKA “congestive adenopathy”). 1-4

Although not as common as alveolar/interstitial edema on chest CT scan, hypertrophy of mediastinal lymph nodes may occur in a significant number of patients with CHF.  In a study involving 215 patients with CHF and no confounding etiology of adenopathy, 68% had evidence of adenopathy, particularly involving the right paratracheal and precarinal, subcarinal and other mediastinal lymph nodes; hilar and single station adenopathy were less common. The findings of pulmonary edema on CT and pleural effusion were significantly associated with adenopathy.1

In a study involving 3 patients with mediastinal adenopathy and CHF, lymph node biopsy showed noninflammatory, benign lesions that did not affect the node structure. Follow-up CT scan in 2 patients at 8 and 10 months showed no changes in the morphologic characteristics of mediastinal lymph nodes, while in another patient most of the enlarged lymph nodes disappeared at 5 months post- acute phase of the CHF.2   Interestingly, another study involving 31 cases of “subacute left heart failure” found that average ejection fraction was lower among patients with adenopathy (34% vs 43%).3

One potential mechanism for CHF-related adenopathy is that the excess lung fluid causes increased flow of fluid through the lymphatic channels and into the lymph nodes resulting in their congestion and enlargement.1

 

Bonus Pearl: Did you know that experimental animal studies have shown that acute CHF is associated with significant increases in mediastinal lymphatic flow and lymphatic vessel dilatation? 4-5

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References

  1. Shweihat YR, Perry J, Etman Y, et al. Congestive adenopathy: A mediastinal sequela of volume overload. J Bronchol Intervent Pulmonol 2016; 23:298-302. https://pubmed.ncbi.nlm.nih.gov/27623420/
  2. Ngom A, Dumont P, Diot P, et al. Benign mediastinal lymphadenopathy in congestive heart failure. CHEST 2001;119: 653-656. https://pubmed.ncbi.nlm.nih.gov/11171755/
  3. Chabbert V, Canevet G, Baixas C, et al. Mediastinal lymphadenopathy in congestive heart failure: a sequential CT evaluation with clinical and echocardiographic correlations. Eur Radiol 2004;14:881-889. https://pubmed.ncbi.nlm.nih.gov/14689226/
  4. Drake RE, Dhother S, Teague RA, et al. Lymph flow in sheep with rapid cardiac ventricular pacing. Am J Physiol 1997; 272:1595-1598. https://pubmed.ncbi.nlm.nih.gov/9176352/
  5. Leeds SE, Uhley HN, Telesky LB. Direct cannulation and injection lymphangiography of the canine cardiac and pulmonary efferent mediastinal lymphatics in congestive hart failure. Invest Radiol 1981;16:193-200. https://pubmed.ncbi.nlm.nih.gov/6266975/

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!

Chest CT scan of my patient with congestive heart failure (CHF) and shortness of breath shows mediastinal adenopathy.  Can mediastinal adenopathy be caused by CHF alone?

Is lung ultrasound useful in evaluating patients with dyspnea?

FA Manian MD, MPH, , , , , , , , , , , , Leave a comment

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

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

 

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/ 
  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/ 
  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/ 
  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 

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?

Is compression therapy for leg edema harmful in patients with congestive heart failure?

FA Manian MD, MPH, , , , , , , , , Leave a comment

The evidence to date, albeit based on small non-randomized studies, suggests that compression therapy of lower extremities in stable patients with congestive heart failure (CHF) is not associated with clinical deterioration, while more studies are needed to evaluate its safety in advanced classes of CHF (NYHA III and IV). The theoretical concern is that by mobilizing fluid from lower extremities, compressive therapy could lead to worsening pulmonary edema in patients with less stable CHF. 1,2

A study of subjects with NYHA II CHF wearing compression stockings found a significant increase in human atrial natriuretic peptide (hANP) in patients with known heart disease but the rise was only transient and not accompanied by hemodynamic changes or clinical deterioration.3 Similar findings have been reported by studies involving patients with NYHA III and IV CHF involving compressive therapy which demonstrated no clinically significant deleterious effects. 4-5

Nevertheless, isolated reports of acute pulmonary edema following compressive therapy in the literature, 6,7 and the theoretical concern raised above have often led to recommendations against the use of CT in patients with advanced CHF. 1,2 We clearly need more studies to evaluate the risks vs benefits of CT in patients with CHF.

Bonus Pearl: Did you know that compressing the legs with pressures of 25 mm Hg and 50 mm Hg can reduce the blood volume in legs by 33% and 38%, respectively? 2

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References

  1. Urbanek T, Jusko M, Kuczmik WB. Compression therapy for leg oedema in patients with heart failure. ESC Heart Failure 2020;7:2012-20. https://onlinelibrary.wiley.com/doi/10.1002/ehf2.12848
  2. Hirsch T. Oedema drainage and cardiac insufficiency—When is there a contraindication for compression and manual lymphatic drainage? Phlebologie 2018;47:115-19. https://www.thieme-connect.de/products/ejournals/pdf/10.12687/phleb2420-3-2018.pdf?articleLanguage=en
  3. Galm O, Jansen-Genzel W, von Helden J, et al. Plasma human atrial natriuretic peptide under compression therapy in patients with chronic venous insufficiency with or without cardiac insufficiency. Vasa 1996;25:48-53. https://pubmed.ncbi.nlm.nih.gov/8851264/
  4. Wilputte F, Renard M, Venner J, et al. Hemodynamic response to multilayered bandages dressed on a lower limb of patients with heart failure. Eur J Lymphology 2005;15:1-4. https://www.researchgate.net/profile/Olivier_Leduc/publication/287602727_Hemodynamic_response_to_multilayered_bandages_dressed_on_a_lower_limb_of_patients_with_heart_failure/links/5704dff008ae44d70ee12eb5/Hemodynamic-response-to-multilayered-bandages-dressed-on-a-lower-limb-of-patients-with-heart-failure.pdf?origin=publication_detail
  5. Leduc O, Crasset V, Leleu C, et al. Impact of manual lymphatic drainage on hemodynamic parameters in patients with heart failure and lower limb edema. Lymphology 2011;44:13-20. https://pubmed.ncbi.nlm.nih.gov/21667818/
  6. Vaassen MM. Manual lymph drainage in a patient with congestive heart failure: a case study. Ostomy Wound Management 2015;61:38-45. https://www.o-wm.com/article/manual-lymph-drainage-patient-congestive-heart-failure-case-study
  7. McCardell CS, Berge KH, Ijaz M, et al. Acute pulmonary edema associated with placement of waist-high, custom fit compression stockings. Mayo Clin Proc 1999;74:478-480. https://www.mayoclinicproceedings.org/article/S0025-6196(11)64822-2/fulltext

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!

Is compression therapy for leg edema harmful in patients with congestive heart failure?

How can I distinguish cardiac asthma from typical bronchial asthma?

FA Manian MD, MPH, , , , , , , , Leave a comment

Certain clinical features of cardiac asthma, defined as congestive heart failure (CHF) associated with wheezing, may be useful in distinguishing it from bronchial asthma, particularly in older patients with COPD (1-3).

• Paroxysmal nocturnal dyspnea associated with wheezing
• Presence of rales or crackles, ascites or other signs of CHF
• Poor response to bronchodilators and corticosteroids
• Formal pulmonary function test with bronchoprovocation demonstrating minimal methacholine response.

Cardiac asthma is not uncommon. In a prospective study of patients 65 yrs of age or older (mean age 82 yrs) presenting with dyspnea due to CHF, cardiac asthma was diagnosed in 35% of subjects. Even in non-elderly patients, cardiac asthma has been reported in 10-15% of patients with CHF (2).

The mechanism(s) underlying cardiac asthma is likely multifactorial. Pulmonary edema and pulmonary vascular congestion have traditionally been considered as key factors either through edema in the interstitial fluid of bronchi squeezing the bronchiolar lumen or by externally compressing the entire airway structure and the bronchiole wall. Reflex bronchoconstriction involving the vagus nerve, bronchial hyperreactivity, systemic inflammation, and airway remodeling may also play a role (1,3). 

Treatment of choice for cardiac asthma typically includes diuretics, nitrates and morphine, not bronchodilators or corticosteroids (1,3). 

Bonus Pearl: Did you know that the term “cardiac asthma” was first coined by the Scottish physician, James Hope, way back in 1832 to distinguish it from bronchial asthma!

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References
1. Litzinger MHJ, Aluen JKN, Cereceres R, et al. Cardiac asthma: not your typical asthma. US Pharm. 2013;38:HS-12-HS-18. https://www.uspharmacist.com/article/cardiac-asthma-not-your-typical-asthma
2. Jorge S, Becquemin MH, Delerme S, et al. Cardiac asthma in elderly patients: incidence, clinical presentation and outcome. BMC Cardiovascular Disorders 2007;7:16. https://www.ncbi.nlm.nih.gov/pubmed/17498318
3. Tanabe T, Rozycki HJ, Kanoh S, et al. Cardiac asthma: new insights into an old disease. Expert Rev Respir Med 2012;6(6), 00-00. https://www.ncbi.nlm.nih.gov/pubmed/23234454

How can I distinguish cardiac asthma from typical bronchial asthma?

Should I avoid intravenous furosemide for management of ascites in my patient with cirrhosis?

FA Manian MD, MPH, , , , , , , , , , Leave a comment

Generally, yes! IV furosemide for treatment of ascites in patients with cirrhosis should be avoided for couple of reasons.

First, in contrast to patients with congestive heart failure in whom the absorption of oral furosemide may be impaired due to bowel wall edema, patients with cirrhosis and ascites appear to absorb oral furosemide efficiently, similarly to that of control patients.1   Another reason for avoiding IV furosemide in this setting is the possibility of a significant drop in the GFR with its attendant rise in BUN and serum creatinine, clinically resembling a picture of hepatorenal syndrome.2

Although the mechanism of the adverse effect of IV furosemide on the renal function of patients with cirrhosis is not totally clear, furosemide-induced vasoconstriction, not intrasvascular volume depletion due to sodium wasting, seems to play an important role.3

Nevertheless, certain situations may necessitate the use of IV furosemide in patients with cirrhosis and ascites, such as in single doses to help identify patients who will be responsive to diuretics, and in patients in need of prompt diuresis such as those with concurrent pulmonary edema. In a somewhat reassuring study, a single dose of 80 mg IV furosemide reliably identified cirrhotic patients with ascites responsive to diuretics, without a significant risk of deteriorating renal function.3

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References

  1. Sawhney VK, Gregory PB, Swezey SE, et al. Furosemide disposition in cirrhotic patients. Gastroenterology 1981; 81: 1012-16. https://www.ncbi.nlm.nih.gov/pubmed/7286579
  2. Daskalopoulos G, Laffi G, Morgan T, et al. Immediate effects of furosemide on renal hemodynamics in chronic liver disease with ascites. Gastroenterology 1987;92:1859-1863. https://www.ncbi.nlm.nih.gov/pubmed/3569760
  3. Spahr, L., Villeneuve, J., Tran, H. K., & Pomier-Layrargues, G. Furosemide-induced natriuresis as a test to identify cirrhotic patients with refractory ascites. Hepatology 2001;33:28-31. https://www.ncbi.nlm.nih.gov/pubmed/11124817

 

Contributed by Sam Miller, MD, Mass General Hospital, Boston, MA.

 

Should I avoid intravenous furosemide for management of ascites in my patient with cirrhosis?

My patient with acute exacerbation of heart failure and pulmonary edema also has pneumonia. How often do heart failure and pneumonia coexist?

FA Manian MD, MPH, , , Leave a comment

More often than you might think! The relationship between pneumonia and heart failure (HF) appears bidirectional with pneumonia precipitating heart failure (HF) and HF predisposing to it.

Although It’s often quoted that acute respiratory tract infection accounts for 3-16% of patients hospitalized with decompensated heart failure (HF) (based primarily on small observational studies),1 a 2016 large prospective study involving nearly 100,000 HF admission from 305 US hospitals has reported “pneumonia/respiratory process” as the most common precipitating clinical factor, present in 28.2% of cases (arrhythmia and medication noncompliance came in as 2nd and 3rd).2

Interestingly, the same study reported that pneumonia/respiratory process was most prevalent among patients with preserved (≥50%) ejection fraction (EF) compared to those with borderline ( 40%-49%) or reduced (<40%) EF (33% vs 30% vs 24%, respectively). 2

Pulmonary edema may in turn predispose to bacterial pneumonia through adverse effects of edema fluid on lung bacterial defense mechanisms and establishment of a culture medium for bacterial growth by the presence of fluid in the alveolar space.3

So don’t be surprised if you have to treat for both!

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

References

  1. Thomsen RW, Kasatpibal N, Riis A, et al. The impact of pre-existing heart failure on pneumonia prognosis: Population-based cohort study. J Gen Intern Med 2008;23:1407-13. https://www.ncbi.nlm.nih.gov/pubmed/18574639
  2. Kapoor JR, Kapoor R, Ju C, et al. Precipitating clinical factors, heart failure characterization, and outcomes in patients hospitalized with heart failure with reduced, borderline, and preserved ejection fraction. JACC 2016;4:464-72. https://www.scholars.northwestern.edu/en/publications/precipitating-clinical-factors-heart-failure-characterization-and 
  3. Harris GD, Woods DE, Fine R, et al. The effect of intraalveolar fluid on lung bacterial clearance. Lung 1980; 158;91-100 Harris GD, Woods DE, Fine R, et al. The effect of intraalveolar fluid on lung bacterial clearance. Lung 1980; 158;91-100. https://link.springer.com/article/10.1007/BF02713708

 

 

My patient with acute exacerbation of heart failure and pulmonary edema also has pneumonia. How often do heart failure and pneumonia coexist?

Should I order serum procalcitonin on my patient with suspected infection?

FA Manian MD, MPH, , , , , , , , , , , 2 Comments

Two things to ask before you order procalcitonin (PCT): 1. Will it impact patient management?; and 2. If so, will the result be available in a timely manner ie, within hours not days?

Whatever the result, PCT should always be interpreted in the context of the patient’s illness and other objective data. Not surprisingly then, as a “screening” test, PCT may be more useful in patients with low pre-test likelihood of having bacterial infection, not dissimilar to the use of D-dimer in patients with low pre-test probability of pulmonary embolism1.  

Several potential clinical uses of this biomarker have emerged in recent years,  including:1,2

  • Helping decide when to initiate antibiotics in patients with upper acute respiratory tract infections and bronchitis. A normal or low PCT supports viral infection.
  • Helping decide when to discontinue antibiotics (ie, when PCT normalizes) in community-acquired or ventilator-associated pneumonia.
  • Helping monitor patient progress with an expected drop in PCT of about 50% per day (half-life ~ 24 hrs) with effective therapy.

Few caveats…

  • PCT may be unremarkable in about a third of patients with bacteremia (especially due to less virulent bacteria, including many gram-positives)3.  
  • PCT levels are lowered by high-flux membrane hemodialysis, so check a baseline level before, not after, hemodialysis4.
  • Lastly, despite its higher specificity for bacterial infections compared to other biomarkers such as C-reactive protein, PCT may be elevated in a variety of non-infectious conditions, including pancreatitis, burns, pulmonary edema or aspiration, mesenteric infarction (ischemic bowel), cardiogenic shock, and hypotension during surgery2.

 

References:

  1. Schuetz P, Muller B, Chirst-Crain M, et al. Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections (review). Evid-Based Child Health (A Cochrane Review Journal) 2013;8:4;1297-137. http://onlinelibrary.wiley.com/doi/10.1002/ebch.1927/pdf
  2. Gilbert GN. Use of plasma procalcitonin levels as an adjunct to clinical microbiology. J Clin Microbiol 2010;48:2325-29. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2897488/pdf/0655-10.pdf
  3. Yan ST, Sun LC, Jia HB. Procalcitonin levels in bloodstream infections caused by different sources and species of bacteria. Am J Emerg Med 2017;35:779-83. https://www.ncbi.nlm.nih.gov/m/pubmed/27979420/#fft
  4. Grace E, Turner RM. Use of procalcitonin in patients with various degrees of chronic kidney disease including renal replacement therapy. Clin Infect Dis 2014;59:1761-7. https://www.ncbi.nlm.nih.gov/pubmed/25228701
Should I order serum procalcitonin on my patient with suspected infection?

When evaluating for an esophageal perforation, is a water-soluble contrast agent such as Gastrografin a better and safer alternative to barium swallow study?

FA Manian MD, MPH, , , , , , , , Leave a comment

Water-soluble contrast agents (WCAs) (eg, meglumine diatrizoate or Gastrografin) are often ordered as the initial radiographic test for evaluation of esophageal perforation or leaks, followed by barium swallow if the test is negative because small leaks are better detected with the more radiopaque barium1.  Such practice, however, is based on extrapolation of data on the deleterious effect of barium when extravasated into the peritoneal cavity, not the mediastinum1.   In fact, clinical evidence linking mediastinitis to extravasated barium is lacking, and even in experimental studies, injection of barium into the mediastinum of cats have failed to cause clinically significant mediastinitis2.

When ordering a contrast swallow study, no medium should be considered totally safe or effective in detecting esophageal perforations or leaks and WCAs are no different. Potential disadvantages of WCAs include: 1. Inferior sensitivity (as low as 50%)—due to decreased radio-opacity—when compared to barium3; 2. Risk of pulmonary edema—occasionally lethal— when aspirated into the lung due to high osmolality (analogous to salt water drowning) and intense inflammatory reaction4,5; 3. Contraindication in the setting of tracheoesophageal fistula,6; 4. Risk of serious allergic reaction due to reabsorption of iodinated compounds1; and 5. Added exposure to radiation and cost of testing when the swallow study is repeated with barium.  For these reasons, the standard practice of an initial WCA followed by a barium swallow`study if the former is negative, has been questioned, with some centers foregoing the WCA study altogether in favor of barium swallow in certain patients 1,6.

In short, when evaluating for esophageal perforation, WCAs should not categorically be considered a “better” or “safer” alternative to barium; in certain situations, barium may be the preferred agent. When in doubt, input from a thoracic surgeon is recommended.  

 

References

  1. Gollub MJ, Bains MS. Barium sulfate: a new (old) contrast agent for diagnosis of postoperative esophageal leaks. Radiology 1997;202:360-62. https://www.ncbi.nlm.nih.gov/pubmed/9015057
  2. James AE, Montali RJ, Chaffee V, et al. Barium or gastrografin: which contrast media for diagnosis of esophageal tears? Gastroenterology 1975;68:1103-1113. https://www.ncbi.nlm.nih.gov/pubmed/1126592
  3. Berry BE, Ochsner JL. Perforation of the esophagus: a 30 year review. J Thorac Cardiovasc Surg 1973;65:1-7. http://www.jpedsurg.org/article/0022-3468(73)90248-0/abstract
  4. Trulzsch DV, PenmetsaA, Karim A, et al. Gastrografin-induced aspiration pneumonia: A lethal complication of computed tomography. South Med J 1992;85:1255-56. https://www.ncbi.nlm.nih.gov/pubmed/1470976
  5. Tuladhar R, Patole S, Whitehall J. Gastrografin aspiration in a neonate with tracheoesophageal fistula. J Paediatr Child Health 2000; 36:94-6. https://www.ncbi.nlm.nih.gov/pubmed/10723703
  6. FDA https://www.drugs.com/pro/gastrografin.html.
  7. Roh S, Iannettoni MD, Keech JC, et al. Role of barium swallow in diagnosing clinically significant anastomotic leak following esophagectomy. Korean J Thorac Cardiovasc Surg 2016;49:99-109. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4825910/pdf/kjtcv-49-099.pdf

 

When evaluating for an esophageal perforation, is a water-soluble contrast agent such as Gastrografin a better and safer alternative to barium swallow study?

My patient on methadone complains of lower extremity edema. Could they be related?

FA Manian MD, MPH, , , , , Leave a comment

Yes! As early as 1979, case series of patients on methadone developing peripheral edema within 3-6 months of therapy appeared in the literature1.  

Subsequent studies revealed that edema may develop from 1 week  to 6 months or longer following initiation of methadone, its severity is dose-dependent, and that it improves with reduction of methadone dose or discontinuation of therapy.  Distal extremities or the face are often involved and pulmonary edema may also occur1-3.  It is often resistant to diuretics.

The mechanism by which methadone causes peripheral edema is unclear but several hypotheses have been forwarded. The high volume of distribution and accumulation of methadone in tissues results in higher oncotic pressures in the extravascular space which in combination with reduced oncotic pressures in blood vessels due to venodilatation may lead to edema.  Other potential mechanisms include opioid-induced histamine release directly from mast cells causing venous permeability, and opioid-induced secretion of antidiuretic hormone 1-3.  

 

If you liked this post, sign up under MENU and get future pearls right into your mailbox!

References

  1. Dawson C, Paterson F, McFatter F, Buchanan D. Methadone and oedema in the palliative care setting: a case report and review of the literature. Scottish Med J 2014;59: e-11-e14. https://www.ncbi.nlm.nih.gov/pubmed/24676025.  
  2. Mahè I, Chassany O, Grenard A-S, Caulin C, Bergmann J-F. Methadone and edema: a case-report and literature review. Eur J Clin Pharmacol 2004;59:923-924. \https://www.deepdyve.com/lp/springer-journals/methadone-and-edema-a-case-report-and-literature-review-PfvnmhB1ia
  3. Kharlamb V, Kourlas H. Edema in a patient receiving methadone for chronic low back pain. Am J Health-Syst Pharm 2007;64:2557-60.https://www.ncbi.nlm.nih.gov/pubmed/18056943

 

My patient on methadone complains of lower extremity edema. Could they be related?

What is the utility of pulmonary auscultation for crackles (rales) in diagnosing congestive heart failure (CHF) or pneumonia?

FA Manian MD, MPH, , , , , , 1 Comment

The evidence for the accuracy of crackles in CHF is not as robust as often assumed, with wide variations in its sensitivity (13%-70%), specificity (35%-100%), positive predictive value (19%-100%), and negative predictive value (17%-85%) (1).

In a study  of patients at high risk for CHF but without valvular heart disease, symptoms of CHF, or comorbid pulmonary disease,  the prevalence of baseline crackles in one or both lungs increased with age: 45-64 y , 11%; 65-79 y, 34%; and 80-95 y, 70%.  At best, fair or poor positive and negative likelihood ratios (LRs) have been reported for crackles in CHF (3.4, and 0.8, respectively) (2). 

The accuracy of crackles in diagnosing pneumonia in patients with cough and fever is not much better: sensitivity 19-67%, specificity 36-94%, and poor positive and negative LRs (1.8 and 0.8, respectively) (2).

So don’t overestimate the accuracy of crackles in CHF or pneumonia, especially if your suspicion for these conditions is high!

If you like this post, sign up under MENU and get future fresh pearls straight into your mailbox!

References

  1. Kataoka H, Matsuno O. Age-related pulmonary crackles (rales) in asymptomatic cardiovascular patients. Ann Fam Med 2008;6:239-245.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2384982/ 
  2. McGee S. Auscultation of the lungs. In Evidence-based physical diagnosis (3rd ed.). Elsevier Saunders, Philadelphia, 2012.
What is the utility of pulmonary auscultation for crackles (rales) in diagnosing congestive heart failure (CHF) or pneumonia?