Fluid Overload Essentials
Get your clinical juices flowing and master the diagnosis and management of patients with fluid overload with this course.
3 CME credits
The physical exam for edema seems easy, but a few tricks can give you additional insights. In this video, watch our expert use the findings to narrow down his differential diagnosis.
With this course, you'll get your clinical juices flowing and master the diagnosis and management of patients with fluid overload. Many diseases can lead to symptomatic fluid overload in hospitalized and ambulatory patients. This course will make you a pro at the diagnosis and management of patients with fluid overload. You’ll learn how to manage complex patients, including those with kidney or other organ dysfunction, and by the end, you will be able to care for patients with fluid overload better than your colleagues can!
There are many possible diagnoses for edema based on the starling equation. When a patient presents with edema how will we determine the cause amongst all these options? We can start by asking ourselves is the edema pitting or non pitting? Remember that edema occurs when fluid in the interstitial space is primarily expanded by isotonic fluid and is very low in proteins. To test for pitting edema, apply gentle pressure to the part of the patient's body that has accumulated edema.
If there is an indentation that remains in place after you remove your finger, it is pitting edema. If there is not an indentation, it is non pitting edema. Often the best place to perform this assessment is right over the tibia in the lower extremities. In pitting edema, this excess of fluid in the interstitial space is usually due to venous occlusion or an elevated central venous pressure that is caused an increase in the capillary hydrostatic pressure. Another cause could be that the patient has hypoalbuminemia which is causing a decrease in the capillary oncotic pressure.
In non pitting edema, the excess fluid is either caused by decreased lymphatic drainage called lymphedema, or a systemic disease like hypothyroidism for example, which leads to myxedema. Both are the result of excess interstitial proteins and connective tissue. Pitting edema can occur in the early stages of lymphedema, but it will eventually become chronic non pitting edema because of the tissue fibrosis that develops. Lymphedema causes the skin to appear doughy and it will not form pits when you apply pressure.
At the very late stages of lymphedema, the skin can become fibrotic, thickened and varicose which means wart like. To assess for lymphedema, we can test for stemmers sign, in this maneuver, you pinch the skin overlying the second metatarsal. Some experts will also pinch the skin over the dorsum of the foot immediately proximal to the second metatarsal instead. If the examiner cannot successfully pinch the skin, then that would be a positive stemmers sign. A positive sign means that the patient likely has lymphedema.
One publication showed that this test has a sensitivity of 92% and a specificity of 57% for lymphedema. Whereas lymphedema is caused by an obstruction in the lymphatic system, myxedema is caused by the accumulation of connective tissue molecules in soft tissues. Severe hypothyroidism, for example can cause myxedema that presents his dry thickened skin with non pitting edema, and a yellow to orange discoloration. Localized pretibial mix edema is often seen in patients with Graves disease.
While we're on the subject of non pitting edema, chronic venous insufficiency is another condition that results in tough, discolored skin. Because of hemosiderin deposition, that skin can have a dark brown or reddish color and as this progresses, the skin gets quite sclerotic and hyper pigmented. Swelling in the absence of pitting points to interstitial protein accumulation and subcutaneous tissue fibrosis. After we have evaluated whether it is pitting or non pitting edema, we move on to ask how the edema is distributed. Is it unilateral, bilateral, or diffusely distributed throughout the body. When it is diffusely distributed throughout the body, it is called an anasarca. We will discuss this further in part two of this lesson.