We have seen our esteemed guests, and they are us! Paul Williams (@PaulNWilliamz) leads the discussion with Matt Watto (@DoctorWatto) and Beth “Garbs” Garbitelli (@bethgarbitelli) on the evaluation and management of common causes of edema.
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Show Segments
Intro, disclaimer
Picks of the Week*
The case of Lynn Fedema
Pathophysiology of edema
Differential diagnosis of chronic edema
Chronic edema work-up
Management of chronic edema
Calvin Fedema and acute edema
Evaluation of acute edema
Outro
Edema Pearls
The pathophysiology behind edema is an imbalance between oncotic pressure and hydrostatic pressure within the venous system.
Chronic venous insufficiency is the most common cause of chronic lower extremity edema, especially in older patients.
Again, bilateral lower extremity cellulitis is extremely uncommon.
Edema may be a sign cardiopulmonary, renal, hepatic, or thyroid dysfunction – so look at the patient in front of you and evaluate for risk factors.
Lymphedema results from impairment of lymphatic return, and can sometimes be distinguished from other causes of edema by the Stemmer sign.
Medications are a common cause of lower extremity edema – don’t forget about the gabapentinoids!
May-Thurner syndrome is caused by anatomical compression of the left iliac vein, and can result in unilateral edema or recurrent deep vein thrombosis.
Acute edema can be caused by deep vein thrombosis, cellulitis, or ruptured popliteal cyst, all of which may be difficult to differentiate from each other.
The physical examination should be directed at finding underlying systemic causes of lower extremity edema.
Management of edema usually includes compression, elevation, and avoidance of exacerbating medications.
Lower Extremity Edema Notes
Edema – Pathophysiology
Generally speaking, venous circulation maintains a balance between hydrostatic pressure and oncotic pressure. Edema can result from perturbations in these forces (Trayes et al 2013).
Increased hydrostatic pressure
Venous hypertension from right-sided heart failure, venous insufficiency, constrictive pericarditis, etc.
Low-protein states like nephrotic syndrome, hepatic failure, protein-energy malnutrition
Capillary dilation
Vasodilation from warmer weather
Inflammatory states such as burns or cellulitis
Additionally, as Cardi B teaches us, a lot of things need to be working for effective venous return. Recall that venous return is largely a passive process and requires functional valves and muscle contraction. Defects in either of these can result in diminished venous return, increased venous pressure, and resultant edema.
Includes stroke, multiple sclerosis, and even lumbar radiculopathy
Determining the Cause – Acute Edema
Deep vein thrombosis
Likelihood can be predicted by calculating Wells score
Generally requires ultrasonography for diagnosis
Cellulitis
Clinically difficult to differentiate from DVT
Ruptured popliteal cyst
Classically presents with ecchymosis around the ankle
Again, may be clinically challenging to differentiate from other causes
Ultrasonography usually required to make the diagnosis
Edema – The Workup
Physical Examination
Assess for symptoms of cardiac disease
Assess for JVD
Pitting edema can be extensive and extend proximally to the sacrum in heart failure
Evaluate for pitting versus non-pitting
Non-pitting edema seen in lymphedema
Check for Stemmer’s sign to evaluate for lymphedema
Inability to pinch the skin at the base of the toes due to skin changes
Evaluate for superimposed cellulitis if chronic changes of venous insufficiency are seen
Laboratory evaluation
Reasonable to check urine protein-creatinine ratio
In most patients, could consider comprehensive metabolic panel to evaluate albumin and electrolyte abnormalities
TSH often checked to rule out thyroid causes
Additional testing, such as urinalysis, complete blood count, BNP, or D-dimer, could be considered depending on patient history and risk factors
Other studies
Venous ultrasound studies should be ordered if there is suspicion for DVT
Consider a transthoracic echocardiogram in patients with cardiopulmonary symptoms
Polysomnography is appropriate for patients for whom there is high suspicion for sleep apnea
Abdominopelvic imaging may be appropriate when the cause is not fully elucidated and there is suspicion for malignancy or other compressive or obstructive etiology
Edema – Management
General principles
Stop exacerbating medications, if possible
Compression stockings are generally helpful, especially for chronic venous insufficiency
Avoid if arterial insufficiency is suspected
Elevate the legs when possible
Diuretics may not be helpful in the absence of volume overload
They are not effective at mitigating edema caused by calcium channel blockers
Patient education and reassurance are an important component of management
There is some evidence for horse chestnut seed extract in the short-term treatment of chronic venous insufficiency (Pittler and Ernst 2012)
Lymphedema management
Best managed by a multidisciplinary team
Usually includes physical therapy and vascular surgery teams
Patients typically undergo complex decongestive physiotherapy
Primary care provider role is to help provide meticulous skin care and ensure care coordination
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Goal
Listeners will explain the basic pathophysiology, diagnosis, and management of common causes of lower extremity edema.
Learning objectives
After listening to this episode listeners will…
Recognize the basic pathophysiology underlying lower extremity edema.
Develop a realistic differential diagnosis for causes of chronic and acute lower extremity edema.
Outline the initial diagnostic work-up of lower extremity edema.
Describe general management principles for common causes of lower extremity edema.
Disclosures
The Curbsiders report no relevant financial disclosures.
Citation
Williams PN. “316 Lower Extremity Edema with The Curbsiders”. The Curbsiders Internal Medicine Podcast. http://thecurbsiders.com/episode-list January 17, 2022.
Comments
January 17, 2022, 11:54am Kenn writes:
Very well know podcasts: informative, just the right length, folksy--but not coming across as fake
Would appreciate an episode on arthritis
Thank you
Loved it! Suggest on infographic the recliner is misleading. To really move fluids out of lower extremities legs need higher than heart. I have patient lay on couch and use cushions to elevate and pump feet to activate calf muscles . I demo in office for them without the pillows-motivation for doc to have string core muscles ! Loved the episode
I wish that the presentation can add the following discussions
1) How to differential lymphedema vs edema
2) Why do two patients with proteinuria could have significantly different degrees of edema. For example, secondary FSGS patients hardly have edema, or primary FSGS patients have awful anasarca.
3) I feel BNP is a very useful tool. If BNP is within the normal range, then the excessive intravascular volume is not the cause of edema. For example, patients with severe pulmonary hypertension can have terrible edema while BNP is normal
You guys mentioned a role for RAS inhibition for reducing leg edema. I'd love to read more about that. Is there a reference you could share?
CME Partner
The Curbsiders are partnering with VCU Health Continuing Education to offer FREE continuing education credits for physicians and other healthcare professionals. Visit curbsiders.vcuhealth.org and search for this episode to claim credit.
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Comments
Very well know podcasts: informative, just the right length, folksy--but not coming across as fake Would appreciate an episode on arthritis Thank you
Thank you for your input! Great topic!
Loved it! Suggest on infographic the recliner is misleading. To really move fluids out of lower extremities legs need higher than heart. I have patient lay on couch and use cushions to elevate and pump feet to activate calf muscles . I demo in office for them without the pillows-motivation for doc to have string core muscles ! Loved the episode
Great info! Thank you for listening!
I wish that the presentation can add the following discussions 1) How to differential lymphedema vs edema 2) Why do two patients with proteinuria could have significantly different degrees of edema. For example, secondary FSGS patients hardly have edema, or primary FSGS patients have awful anasarca. 3) I feel BNP is a very useful tool. If BNP is within the normal range, then the excessive intravascular volume is not the cause of edema. For example, patients with severe pulmonary hypertension can have terrible edema while BNP is normal
We appreciate your feedback!
You guys mentioned a role for RAS inhibition for reducing leg edema. I'd love to read more about that. Is there a reference you could share?