Approach to lower limb edema: Clinical sciences
1,324views

test
00:00 / 00:00
Approach to lower limb edema: Clinical sciences
Core acute presentations
Abdominal pain
Abnormal vaginal bleeding
Acute kidney injury
Anemia
Chest pain
Common skin lesions
Common skin rashes
Constipation
Cough
Dementia (acute symptoms)
Depression (initial presentation)
Diarrhea
Dysuria
Fever
Headache
Joint pain and injury
Leg swelling
Low back pain
Male genitourinary symptoms
Pregnancy (initial presentation)
Red eye
Shortness of breath and wheezing
Upper respiratory symptoms
Vaginal discharge
Assessments
USMLE® Step 2 questions
0 / 4 complete
Decision-Making Tree
Questions
USMLE® Step 2 style questions USMLE
0 of 4 complete
Laboratory Test | Value |
Serum sodium | 130 mEq/L |
Serum creatinine | 2.8 mg/dL |
Serum AST | 228 U/L |
Serum ALT | 112 U/L |
Serum total bilirubin | 3.8 mg/dL |
Serum INR | 1.0 |
Urine protein/creatinine | 0.6 |
Transcript
Edema is an abnormal accumulation of interstitial fluid in the tissues. This occurs due to an imbalance between the hydrostatic and oncotic forces at the level of the capillaries. The lower limbs are especially prone to the development of edema because of gravity.
Based on location and symmetry, lower limb edema can be classified as unilateral and bilateral. Unilateral lower limb edema is usually caused by a pathological process in the limb itself, such as DVT or compartment syndrome, while bilateral lower limb edema is usually due to systemic causes like heart, liver, and kidney failure. A more severe type of edema is anasarca, where the whole body develops generalized edema, and can be caused by things like malnutrition, as well as cirrhosis, nephrotic syndrome, or even burns.
When approaching a patient with lower limb edema, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If your patient is unstable, you should first stabilize their airway, breathing, and circulation before trying to identify the cause. This means that you might need to intubate the patient and establish IV access before continuing with your assessment.
On the other hand, if the patient is stable, the next step is to obtain a focused history and physical examination. Your history should explore if one or both lower limbs are affected, time span over which edema developed, associated symptoms such as pain or shortness of breath, known acute or chronic medical conditions, and a list of medications. Your physical exam should focus on describing the characteristics of the edema, like location, symmetry, and whether it’s pitting or non-pitting, as well as other features like skin discoloration and the quality of the pulse in the affected limbs.
First, let’s start with conditions that cause unilateral edema. Unilateral edema generally affects a single limb and can be acute, that is developing over a period of 72 hours or less, or it might be chronic where it takes longer than 72 hours to develop. You’ll want to rule out potentially life and limb-threatening conditions associated with unilateral edema first.
Let’s take a look at the most important causes of acute-onset unilateral edema. A very important one is DVT, which is a blood clot that develops in the deep veins. Keep this in mind if your patient reports painful swelling, especially in the presence of DVT risk factors, like smoking or oral contraceptive use. Exam might reveal edema, erythema, and warmth, perhaps a difference in calf circumference or a positive Homan sign, which means pain behind the calf when passively dorsiflexed. At this point you should consider DVT, and calculate a Wells score. Additionally, you might need to order a D-dimer and ultrasound. Wells score above 2, elevated D-dimer, and positive ultrasound findings showing a non-compressible deep vein with obstructed flow can confirm the diagnosis of DVT.
Another important differential is cellulitis. This is a bacterial skin infection involving dermis and subcutaneous tissue. The patient may develop painful swelling, often associated with fever. If your examination shows erythema, warmth, induration, or abscess formation, then your patient most likely has cellulitis. While this is a clinical diagnosis, you may want to order a CBC, and to collect any drainage or purulence from the affected area to send for culture. Elevated WBC and positive cultures support the diagnosis of cellulitis.
Next up is compartment syndrome. The edema here is contained within fascial compartments, leading to a limb-threatening rise in intracompartmental pressures. In this case, there’s usually a history of recent trauma, surgery, or burn; while a physical exam reveals the 6 Ps: pain, pallor, paresthesia, pulselessness, paralysis, and poikilothermia. These findings are highly-suggestive of compartment syndrome, which is usually a clinical diagnosis. To support the diagnosis, you may measure intracompartmental pressures and order labs, such as serum creatine phosphokinase, or CPK, and urine myoglobin, all of which would be elevated.
Finally, there’s Baker cyst rupture. Baker cyst is a collection of synovial fluid that develops in the popliteal fossa that can rupture and drain into the lower leg, causing edema. History typically reveals a previous knee injury or osteoarthritis, while physical exam findings usually include redness, warmth, and sometimes a palpable cyst in the popliteal fossa. At this point, you should consider Baker cyst rupture. You can confirm the diagnosis with an MRI showing an intermuscular fluid collection.
Sources
- "The American Venous Forum, American Vein and Lymphatic Society and the Society for Vascular Medicine expert opinion consensus on lymphedema diagnosis and treatment" Phlebology (2022)
- "Standard of care for lipedema in the United States" Phlebology (2021)
- "Edema: diagnosis and management" Am Fam Physician (2013)
- "The Renal System" ClinicalKey Student (2022)
- "Approach to leg edema of unclear etiology" J Am Board Fam Med (2006)
- "ABC of arterial and venous disease. Swollen lower limb-1: general assessment and deep vein thrombosis" BMJ (2000)
- "Diagnosis and management of lymphatic vascular disease" J Am Coll Cardiol (2008)