Not All Swelling Is Equal: Differential Diagnosis of Edemas
This article is the first in a series of three that will address the clinical importance of recognizing edema for differential diagnosis. The focus of this article will be on recognizing edema and performing appropriate clinical tests to help with clinical diagnosis. The second article will focus on the pathophysiology of lymphedema, and the third article will cover common complications seen with lymphedema.
Edema is a common condition many of us have experienced. It is seemingly benign and self-limiting. By definition, edema is the presence of abnormal amounts of fluid in the extracellular tissues. Typically, an equilibrium is maintained through a delicate balance between hydrostatic and osmotic pressure inside and outside the blood vessels.
Generally speaking, hydrostatic pressure is determined by blood pressure and the effects of gravity, whereas osmotic pressure is determined by the concentration of protein inside and outside the vessels. Under normal circumstances, the hydrostatic pressure that pushes fluid out of the veins is slightly higher than the osmotic pressure that keeps fluid in. This results in a slight loss of fluid into the interstitial space. Subsequently, this fluid is taken up by the lymphatic capillaries and returned to the venous circulation as lymphatic fluid. Daily fluctuations exist, but for the most part, the human body does an exceptional job maintaining fluid balance.
This may seem straightforward, but it isn’t. There are more than 30 medical causes of edema, which can range from mild dependent edema to swelling from a minor trauma such as an ankle sprain, to specific disease-related edemas to complex swelling associated with concomitant comorbidities. To help accurately identify the type of edema and determine the underlying pathophysiology and associated complications that patients may have, healthcare providers need to be aware of the clinical presentation of edema and the subtle variations that can exist. Early recognition of the type of edema is essential because not all edemas are managed the same nor benefit from standard interventions. This article will focus on how to clinically assess edema to assist with differential diagnosis and to direct the plan of care by providing the appropriate interventions based on the type of edema presenting.
Initially, it is important to examine the characteristics of the edema and involved tissue structures. The texture of the tissues as well as pitting and rebound qualities of the swelling can assist in differential diagnosis. Edema can present as pitting or nonpitting and can be determined by palpating the involved area or extremity. Pitting edema can be determined by applying firm, yet gentle pressure to the swollen area by depressing the skin with the finger. If the pressing results in an indentation that persists for some time after the release of the pressure, the edema is considered pitting edema. Rebound is the time it takes for the indentation to disappear and can be helpful in determining the severity of the edema. In nonpitting edema, the pressure applied to the skin does not result in an indentation, or the indentation may be difficult to induce and long to rebound. Pitting is indicative of fluid in the tissues, whereas rebound is indicative of fibrotic changes in the tissues.
Pitting edema is graded on a scale of one to four and is determined by the depth of the indentation as well as time to rebound or return to normal. Variations do exist. Table 1 is a culmination of the various pitting scales.
Nonpitting edema is typically indicative of lymphedema due to the fibrotic changes associated with this condition. Fibrosis leads to a hardening of the skin, which renders the tissues unyielding to indentation. In addition to determining the pitting or nonpitting quality of the edema, texture must also be assessed. Tissue texture, in the context of edema, can present on a spectrum or continuum as described in Table 2.
Appreciating the pitting and texture characteristics of the edema will provide valuable insight into the potential underlying cause(s) of the edema. In addition, the tissue temperature should be assessed in the edematous area and compared to contralateral and/or noninvolved area(s) to ascertain whether the temperature is normal, elevated, or cooler to touch. Any deviation from normal should be further investigated and may warrant referral to a physician. Elevated temperatures could be indicative of active inflammation or infection. Cooler temperatures could be related to underlying circulatory impairments or a local ischemia.
|1+||2 mm, barely detectable, pitting rapidly disappears, immediate rebound|
|2+||4 mm, rebound varies from a few seconds to 10-15 seconds|
|3+||6 mm, rebound varies from 10-12 seconds to 30 seconds to 1 minute; extremity appears fuller and swollen|
|4+||8 mm, rebound varies from >20 seconds to 2-5 minutes; extremity is grossly edematous and distorted|
|Normal||Supple, pliable, elastic|
|Watery Edema||Palpation manually displaces fluid; palpable pockets of fluid under thin, translucent skin|
|Soft Pitting Edema||Soft; boggy; feels like dough when palpated or manipulated|
|Fibrotic||Skin thickened, difficult to pinch or tent; difficult to induce pitting or pitting remains >30 seconds; dense connective tissue; less fibrotic —feels like a tube of toothpaste; more fibrotic —feels firms and leathery; skin may have a cobblestone or lumpy, bumpy appearance|
|Hard/ Noncompressible||Nonpitting; nonpliable; appearance akin alligator skin or tree bark; typical of advanced or long-standing lymphedema|
Temperature can be assessed by using one of three methods in clinical practice. The first method is manual assessment by placing the back of the hand on the area in question and comparing it to the contralateral and/or noninvolved area(s) to detect temperature discrepancies. Two other methods involve simple, handheld clinical tools. A thermistor measures surface temperature with a probe that requires surface contact. Thermistors are appropriate on skin that is intact and not denuded or weeping. A radiometer measures surface temperature by infrared radiation. It does not require surface contact and therefore can be used on tissue that is disrupted, impaired, or weeping.
|Etiology||Failure of valves in deep, perforating or superficial veins||Lymph transport failure||Abnormal fat depositions and metabolism (not obesity)||Heart Failure|
|Appearance||Edema in gaiter area||Edematous legs with square-shaped toes, deep folds, loss of contours||Large hips, thighs, feet spared, disproportionately small trunk and arms||Buffalo hump on dorsal feet|
|Texture||Brawny||Lumpy, bumpy or hard, crusty; earlypitting, long- standing nonpitting||Loose, lobular||Soft, doughy, deeply pitting|
|Progression||Distal, below knee||Distal to proximal||Distributed evenly hips and thighs||Distal to proximal|
|Response to Elevation||Reduces||Persists||Unaffected (not a fluid problem)||Reduces rapidly|
|Onset||Slow||Slow||Slow; primarily affects females||Rapid|
|Pain||Achy, worse at end of day||Rarely painful||Painful to palpation||Distention discomfort|
|Wounds||Weeping, blistering, shallow, uncomfortable, venous ulcers common||Ulcers uncommon, lymphorreah with skin denudement common||Bruise easily; no ulcers or weeping||Distention and weeping, watery edema, blisters|
|Skin Changes||Hemosiderin staining, strophe blanche, lipodermatosclerosis, brawny or taut skin, varicose veins, dermatitis||Progressive fibrosis, lichenification, hyperkeratosis, papillomatosis||Bruises easily, weak connective tissue, loose and lobular fatty tissue||Cyanosis, jugular distention, shortness of breath|
|Infection||Rarely cellulitis, can be polymicrobial||Recurrent cellulitis and fungal infections||No cellulitis||No cellulitis|
|Tests and Measures||ABI, venous duplex ultrasound||ABI, venous duplex ultrasound||N/A unless concurrent CVI or lymphedema||ABI ro arterial disease and venous duplex ultrasound to r/o DVT|
|Treatment||Multilayered compression bandaging to reduce, day compression garment to maintain, 30-40 mmHg, wound care||Complete decongestive therapy, diuretics are contraindicated (unless other medical condition warrants use)||Supportive compression garment 20-30 mmHg, diuretics not indicated, may progress to CVI and/or lymphedema; require those interventions||Medical management, diuretics, thigh high compression 20-30 mmHg|
|NOTE: Created by Robyn Bjork, International Lymphedema and Wound Training Institiute. Reprinted with permission. Modified by author.|
Another clinically relevant test is the Stemmer Sign. A thorough physical examination is considered the gold standard for the diagnosis of lymphedema. A complete history, systems review, inspection, and palpation can assist in determining whether the edema is lymphedema. At present, the only clinical test that has been proven reliable and valid to clinically diagnose lymphedema is the Stemmer Sign. The fibrotic changes associated with lymphedema can lead to a thickening of the skin over the proximal phalanges of the toes or fingers. If the clinician is unable to tent or pinch the skin on the involved extremity, this indicates the presence of lymphedema (positive Stemmer Sign as shown in the photo to the right). A negative finding (where the tissue is still pliable and soft), however, does not rule out the presence of lymphedema. It just may be the lymphedema is still in the early stages before tissue proliferation and fibrosis has occurred.
In clinical practice, the most common forms of edema seen are due to congestive heart failure (CHF), deep vein thrombosis (DVT), chronic venous insufficiency (CVI), and lymphedema. Patients with lipedema often are thought to have edematous limbs, even though this condition is not fluid-related but rather a pathological deposition of adipose tissue. An excellent resource to learn more about lipedema can be found at http://www.lipedema-simplified.org/. It is important to note that lymphedema is often complicated by other conditions leading to combination forms of complex swelling. For example, lymphedema with concomitant CVI is plebolymphedema. Lymphedema in patients with lipedema is lipolymphedema. Patients can also present with lymphedema, CVI, and lipedema, which is known as phlebolipolymphedema. A detailed article on lymphedema will follow in the next issue of WCHM magazine. Please refer to Table 3 for a comprehensive overview comparing various edemas.
A thorough patient history should be conducted on any patient presenting with edema of unknown origin. Reviewing the medications the patient is taking is of utmost importance, as many medications can induce or exacerbate swelling.
It is also important to perform noninvasive vascular testing on patients with lower-extremity edema. It is vital to appreciate the health of patients’ venous and arterial systems, as compression is often the cornerstone therapy for edema management. To safely and effectively use compression, healthcare providers must understand if a patient’s body can tolerate compression.
The Ankle Brachial Index (ABI) is a noninvasive vascular exam to screen for arterial insufficiency. It compares blood- flow pressure in the lower leg to blood-flow pressure in the upper arm. By dividing ankle pressure by brachial pressure, a ratio is determined, which is the ABI value. Variations exist in the literature, but the interpretation shown in Table 4 is widely accepted in clinical practice.
|0.8-0.9||Some Arterial Disease||Treat risk factors|
|0.5-0.8||Moderate Arterial Disease||
Refer to vascular specialist (do not compress)
|<0.5||Severe Arterial Disease||
Refer to vascular specialist (do not compress)
Realize, however, that ABI screening may not be accurate in diabetic patients whose vessels are often calcified. Their values tend to be falsely elevated (often > 1.2) and may often be mistaken for normal. Transcutaneous oxygen, tcpO2 or TCOM, and toe pressures are more reliable vascular screens for patients with diabetes.
Comprehensive skin assessment, including a thorough review for edema, should be part of every patient encounter. Recognizing and appreciating the qualities and characteristics of edema will assist healthcare providers with differential diagnosis to promote appropriate interventions and improve patient outcomes.