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

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

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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?

Why is my relatively healthy elderly patient so prone to hyperkalemia?

Hyporeninemic hypoaldosteronism (HH)—without impairment of cortisol synthesis— is associated with hyperkalemic (type IV) renal tubular acidosis (RTA) and is not uncommon among older patients despite glomerular filtration rates (GFRs) >20 ml/min, and absence of diabetes mellitus or chronic tubulointerstitial disease (1-7).  

Hyperkalemia due to HH in the elderly should come as no surprise because the renin-angiotensin-aldosterone system (RAAS) function declines with age, reaching its lowest level by age 60. 1-4   In fact, older people have comparatively lower mean levels of plasma renin and aldosterone at baseline and have an impaired ability to mount appropriate responses to RAAS stimuli, such as upright posture, volume depletion, catecholamines, or potassium administration (3-5).

The impaired RAAS capacity in the elderly often becomes more obvious when they are prescribed medications that further suppress RAAS (3). These include angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, beta-blockers, calcium-channel blockers, nonsteroidal anti-inflammatory agents and heparin (3,7). 

Drugs that increase aldosterone resistance, including potassium-sparing diuretics (eg, spironolactone, amiloride, triamterene, eplerenone) and certain antibiotics (eg, trimethoprim, pentamidine) may also aggravate hyperkalemia associated with HH (7). 

A variety of mechanisms leading to HH with aging have been proposed. These include impaired conversion of prorenin to renin, prostaglandin deficiency, sympathetic nervous system dysfunction and increased plasma levels of atrial natriuretic factors as found in congestive heart failure (1,7). 

Bonus pearl: Did you know that the first case of “pure hypoaldosteronism” was described in 1957 in a 71 year old non-diabetic patient with hyperkalemia in the setting of congestive heart failure? (8)

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References

  1. Bauer JH. Age-related changes in the renin-aldosterone system. Physiological effects and clinical implications. Drugs & Aging 1993;3:238-45. https://www.ncbi.nlm.nih.gov/pubmed/8324299
  2. Musso CG, Jauregui JR. Renin-angiotensin-aldosterone system and the aging kidney. Expert Rev Endocrinol Metab 2014;9:543-46. https://www.tandfonline.com/doi/full/10.1586/17446651.2014.956723
  3. Yoon HE, Choi BS. The renin-angiotensin system and aging in the kidney. Korean J Intern Med 2014;29:291-95. https://www.researchgate.net/publication/262530577_The_renin-angiotensin_system_and_aging_in_the_kidney
  4. Nadler JL, Lee FO, Hsueh W, et al. Evidence of prostacyclin deficiency in the syndrome of hyporeninemic hypoaldosteronism. N Engl J Med 1986;314:1015-20. https://www.ncbi.nlm.nih.gov/pubmed/3515183
  5. Williams GH. Hyporeninemic hypoaldosteronism. N Engl J Med 1986;314:1041-42. https://www.ncbi.nlm.nih.gov/pubmed/3515186
  6.  Block BL, Bernard S, Schwartzstein RM. Hypo-hypo: a complex metabolic disorder. Ann Am Thorac Soc 2016;13:127-133. https://www.ncbi.nlm.nih.gov/pubmed/26730868
  7. Michelis MF. Hyperkalemia in the elderly. Am J Kid Dis 1990;16:296-99.https://www.ajkd.org/article/S0272-6386(12)80005-9/pdf
  8. Hudson JB, Chobanian AV, Relman AS. Hypoaldosteronism. A clinical study of a patient with an isolated adrenal mineralocorticoid deficiency, resulting in hyperkaliemia and Stokes-Adams attack. N Engl J Med 1957;257:529-36. https://www.ncbi.nlm.nih.gov/pubmed/13464977

 

Why is my relatively healthy elderly patient so prone to hyperkalemia?