Difference Between Edema And Inflammation

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Difference Between Edema And Inflammation
What is swelling? – Swelling is any abnormal enlargement of a body part. It is typically the result of inflammation or a buildup of fluid. Edema describes swelling in the tissue outside of the joint. Effusion describes swelling that is inside a joint, such as a swollen ankle or knee.

Hemarthrosis is a condition where there is blood and swelling within a joint. This indicates either a ligament injury, such as an ACL tear or a fracture. Hemarthrosis is determined by removing some fluid from the joint with a needle. Acute refers to swelling that occurs within 24 hours of injury. If the swelling occurs within the first 2 hours, it is probably associated with hemarthrosis and should be checked out by a physician.

Chronic refers to swelling that occurs over a long period of time and can be difficult for an athlete to detect, but is very harmful if left untreated.

Is edema inflammatory?

Acute Inflammatory Edema: A Case Report with Histopathological and Immunohistochemical Findings 1 Division of Dermatology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand Find articles by 1 Division of Dermatology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand Find articles by 1 Division of Dermatology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand Find articles by 1 Division of Dermatology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand Correspondence: Poonkiat Suchonwanit Division of Dermatology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, 270 Rama VI Road, Ratchathewi, Bangkok, 10400, Thailand, Phone: Tel +66-2-2011141, Fax: Fax +66-2-201-1211 ext 4, Email [email protected] Received 2021 Aug 12; Accepted 2021 Sep 11.

© 2021 Chirasuthat et al. This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (). Acute inflammatory edema (AIE) is a rare variant of pseudocellulitis characterized by blanchable, erythematous, and edematous plaques mainly on the thighs and abdomen and sparing areas of increased pressure.

The condition occurs predominantly in critically ill patients with hypoalbuminemia, those with increased body mass index, and those with evidence of fluid overload. AIE was introduced in 2019; however, its histopathological picture has never been elucidated in the literature. We report a case of AIE in a 64-year-old Thai woman with several comorbidities and illustrate its histopathological and immunohistochemical features for the first time.

Treatment with diuretics, fluid restriction, and adjuvant hemodialysis revealed marked improvement after ten days. Our report emphasizes that AIE is a distinct dermatosis with specific characteristics that help differentiate AIE from cellulitis and other pseudocellulitic conditions.

Furthermore, our observations support the role of lymphatic alterations in the pathogenesis of the disease. Keywords: cellulitis, dermis, edema-phage, lymphedema, pseudocellulitis, volume overload Acute inflammatory edema (AIE) is a non-infectious inflammatory skin disorder that is characterized by bilateral, erythematous, edematous plaques, most commonly observed on the dependent parts of the thighs and abdomen, sparing areas of skin subject to pressure.

It is considered to be an under-recognized variant of pseudocellulitis that occurs primarily in critically ill patients. Factors associated with the development of AIE include hypoalbuminemia, obesity, fluid overload, and renal impairment. The pathogenesis of AIE remains unclear; however, acute fluid accumulation in connective tissues causing microtrauma with resultant inflammation is hypothesized.

  1. Since its first description in 2019, to the best of our knowledge, no demonstration of its histopathological picture exists in the literature.
  2. Herein, we describe a case of AIE and illustrate its histopathological and immunohistochemical features for the first time in a Thai patient with several comorbidities.

Our microscopic findings help differentiate AIE from other conditions and highlight the role of the lymphatic system in the pathogenesis of the disease. A 64-year-old woman presented to the hospital with fever, low urine output, dramatic weight gain of 14 kg, and presence of erythematous, edematous rashes on her abdomen and legs for one week.

  1. The patient suffered from several comorbidities, including obesity, obstructive sleep apnea, non-alcoholic fatty liver disease, hypertension, dyslipidemia, chronic kidney disease, and type 2 diabetes mellitus.
  2. She was hospitalized, presumptively diagnosed with cellulitis, and administered empirical antibiotics with ceftriaxone for one week; however, the skin lesions did not respond to the treatment.
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On Day 9 of hospitalization, the dermatology department was consulted for evaluation of her skin lesions. On general examination, the patient was febrile (38.6°C); however, other hemodynamic parameters were normal. Dermatological examination revealed ill-defined, blanchable, erythematous, edematous, mildly tender, warm plaques on the abdomen and lower extremities ().

The skin folds were spared. Laboratory investigations revealed leukocytosis (white blood cell count of 10,310/uL with a differential including 65% neutrophils, 29% lymphocytes, 4% monocytes, and 2% eosinophils), hypoalbuminemia (27.6 g/L), and elevated serum creatinine levels (1.52 mg/dL); these were indicative of acute kidney injury.

The aspartate transaminase, alanine transaminase, gamma-glutamyl transferase, and globulin levels were within normal limits. The blood cultures were negative. Incisional biopsy was performed for microscopic examination, differentiating cellulitis and pseudocellulitic conditions, and further tissue culture for microorganisms.

Histopathological sections showed perivascular and interstitial inflammatory cell infiltration, predominantly in the markedly edematous papillary dermis (). The inflammatory cells comprised lymphocytes, neutrophils, and scattered histiocytes, including edema-phages with bubbly cytoplasm (). The overlying epidermis showed irregular acanthosis with extensive ballooning and keratocyte necrosis in discrete foci.

Vasodilation and moderate erythrocyte extravasation were observed. Furthermore, numerous, large, irregular, thin-walled vascular channels lined by a single layer of flattened endothelial cells were observed (). These vascular spaces appeared empty. ( A ) Histopathology shows perivascular and interstitial inflammatory cell infiltration, predominantly in the markedly edematous papillary dermis (hematoxylin-eosin, original magnification x20); ( B ) Edema-phages, swelling or ballooning of histiocytes, containing either small or large clear vacuoles in their cytoplasm (hematoxylin-eosin, original magnification x400); ( C ) Numerous, large, irregular, thin-walled vascular channels lined by a single layer of flattened endothelial cells (hematoxylin-eosin, original magnification x40); ( D ) Immunohistochemistry reveals positive staining of the ectatic vessel endothelial cells with D2-40 (podoplanin) (original magnification x400).

The immunohistochemical examination revealed positive staining of the ectatic vessel endothelial cells with monoclonal antibodies to D2-40 (podoplanin), which are highly selective lymphatic endothelial markers of lymphatic endothelium; hence, this indicates that the vessels were of a lymphatic nature ().

Edema (Oedema) | In 2 minutes!

Special stains for microorganisms and tissue cultures of the biopsy specimens were negative. Based on her clinical presentation and investigation findings, a diagnosis of AIE was made. We ensured fluid restriction and administered diuretics and adjuvant hemodialysis.

No antibiotics were administered. Ten days following this treatment regimen, the cutaneous lesions showed marked response, and her condition was greatly improved. AIE is an under-recognized variant of pseudocellulitis that is characterized by bilateral, erythematous, edematous plaques on the dependent parts of the body.

The principal differential diagnosis of AIE includes cellulitis and other pseudocellulitic conditions., The pathogenesis of AIE is proposed to be an acute volume overload with impaired lymphatic drainage, leading to microtrauma of the affected connective tissues with the subsequent release of inflammatory cytokines.

Stain and culture of the specimens from skin lesions are recommended to help differentiate cellulitis from its mimicking conditions., AIE was first described by Marchionne et al in a case series of 15 patients; furthermore, they reported that the disease predominantly occurred in patients with a low serum albumin level, fluid overload, a body mass index ≥25 kg.m −2, and renal dysfunction.

They described the skin biopsy findings of three patients, which revealed marked papillary edema and mixed inflammatory cell infiltration comprising neutrophils, lymphocytes, and histiocytes with bubbly cytoplasm (edema-phages) in all specimens; however, they did not provide representative histopathological pictures of these findings.

  • Hence, our case report has demonstrated, for the first time, histopathological images of edema-phages that are described as swelling or ballooning of histiocytes, containing either small or large clear vacuoles in their cytoplasm.
  • Unlike foamy histiocytes (lipid-laden macrophages), they do not contain cholesterol, which is observed as abundant fine granular and/or foamy content in the cytoplasm.

We hypothesize that edema-phages are histiocytes engulfing excess protein and/or fluids in the extracellular space and could be categorized as pathognomonic cells under AIE. Additionally, we observed extensive proliferation of abnormal dilated vascular channels that were later identified as lymphatic vessels, as they showed positive staining with monoclonal antibodies of D2-40 (podoplanin).

  • This finding is crucial for differentiating AIE from cellulitis and other conditions of pseudocellulitis.
  • Abnormal lymphatic channels may play an important role in the pathogenesis of AIE.
  • Following development of volume overload, the impairment of lymphatic drainage may play a role in synergistically promoting extracellular fluid retention in the papillary dermis.

In cases where the process occurs abruptly, microtears may develop in the surrounding connective tissue that may activate the process of inflammation. The primary focus in AIE management is to reduce the excessive amount of body fluid. Hence, fluid restriction, diuretics, hemodialysis, local compression, frequent repositioning, and increased mobility are the recommended treatment modalities.

  1. In the absence of infection, antibiotics are not recommended in AIE.
  2. Misdiagnosis of AIE leads to inappropriate antibiotic administration, increased morbidity, and poor distribution of medical resources.
  3. We describe, for the first time, a case of AIE with histopathological and immunohistochemical findings.
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Despite the rarity of this condition, our report highlights that AIE is a distinct dermatosis with specific characteristics that help differentiate AIE from other conditions. Our observations also reinforce the role of lymphatic abnormalities in the pathogenesis of the disease.

  • No sources of funding were used to prepare this manuscript.
  • This article was performed in accordance with the principles of Declaration of Helsinki.
  • Ethical review and approval was not required to publish the case details in accordance with the local legislation and institutional requirements.
  • Written informed consent was obtained from the patient for publication of this case report and any accompanying images as per our standard institutional rules.

The authors declare that this manuscript was prepared in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The authors report no conflicts of interest in this work.1. Marchionne EM, McCalmont TH, Pincus LB, LeBoit PE, Fox LP.

Acute inflammatory edema: a mimicker of cellulitis in critically ill patients, J Am Acad Dermatol,2019; 81 ( 4 ):931–936. doi: 10.1016/j.jaad.2019.05.083 2. Heymann WR. Acute inflammatory edema: a swell concept, J Am Acad Dermatol,2019; 81 ( 4 ):906–907. doi: 10.1016/j.jaad.2019.07.096 3. Kong LL, Yang NZ, Shi LH, et al.

The optimum marker for the detection of lymphatic vessels, Mol Clin Oncol,2017; 7 ( 4 ):515–520. doi: 10.3892/mco.2017.1356 4. Korniyenko A, Lozada J, Ranade A, Sandhu G. Recurrent lower extremity pseudocellulitis, Am J Ther,2012; 19 ( 4 ):e141–142. doi: 10.1097/01.mjt.0000522273.81146.49 5.

Strazzula L, Cotliar J, Fox LP, et al. Inpatient dermatology consultation aids diagnosis of cellulitis among hospitalized patients: a multi-institutional analysis, J Am Acad Dermatol,2015; 73 ( 1 ):70–75. doi: 10.1016/j.jaad.2014.11.012 6. Surovy AM, Pelivani N, Hegyi I, Buettiker U, Beltraminelli H, Borradori L.

Giant cellulitis-like Sweet syndrome, a new variant of neutrophilic dermatosis, JAMA Dermatology,2013; 149 ( 1 ):79–83. doi: 10.1001/2013.jamadermatol.548 7. Singer S, Li DG, Gunasekera N, et al. The ALT-70 cellulitis model maintains predictive value at 24 and 48 hours after presentation,

J Am Acad Dermatol,2019; 81 ( 6 ):1252–1256. doi: 10.1016/j.jaad.2019.03.050 8. Suchonwanit P, Triamchaisri S, Wittayakornrerk S, Rattanakaemakorn P. Leprosy Reaction in Thai Population: a 20-Year Retrospective Study, Dermatol Res Pract,2015; 2015 :253154. doi: 10.1155/2015/253154 9. Weng QY, Raff AB, Cohen JM, et al.

Costs and consequences associated with misdiagnosed lower extremity cellulitis, JAMA Dermatology,2017; 153 ( 2 ):141–146. doi: 10.1001/jamadermatol.2016.3816 : Acute Inflammatory Edema: A Case Report with Histopathological and Immunohistochemical Findings

Why is inflammation associated with edema?

Abstract – Edema is a swelling from liquid accumulation in body tissues. Injuries in tissues or organs may cause this disorder leading to chemical mediators releasing and triggering the inflammatory process. Inflammatory mediators, when released in response to injuries, promote biological reactions at the affected site.

Furthermore, plasma membrane receptors modulate the inflammatory chemical agent synthesis and release. Pattern recognition receptors, such as Toll Like is an example of plasma membrane receptors associated with chemical agents recognizing and cascade amplification. Therefore, these plasma membrane proteins exhibit essential roles during injuries and immunologic response.

Thus, this review discusses the plasma membrane receptors modulation in the inflammatory area, focusing on edema formation.

Does swelling always mean inflammation?

Swelling – Swelling can occur when a part of the body becomes inflamed. However, it is caused by the accumulation of fluid in tissues throughout the body, or in a specific region of the body. As a result, swelling can actually occur within the body without inflammation occurring. To push the parameters even more, swelling therefore cannot be used as a synonym.

Is inflammation the same as water retention?

Infections and allergies – The immune system’s role is to defend the body from disease and infection. When the immune system detects an unwanted invader, such as bacteria or an allergen, it will mount an attack. Inflammation is part of this process. When inflammation occurs, the body releases histamine.

Histamine causes the gaps between the cells of the capillary walls to widen. It does this to allow infection-fighting white blood cells to reach the site of inflammation. However, it can also allow fluid to leak from the capillaries into the surrounding tissues. The swelling that results from this is usually short-term.

People with long-term inflammation may experience water retention.

Is edema one of the symptoms of inflammation?

Edema in foot and ankle – Swelling of the foot, ankle and leg can be bad enough to leave a dimple, also known as a pit, in the skin after pressing on the area. This swelling, called edema, is the result of too much fluid in the tissues. Congestive heart failure or the vein not working well, also known as venous insufficiency, is often the cause. Symptoms of edema include:

Swelling or puffiness of the tissue right under the skin, especially in legs or arms. Stretched or shiny skin. Skin that holds a dimple, also known as pitting, after it’s been pressed for a few seconds. Increase in the size of the stomach area. Feeling of leg heaviness.

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Will drinking more water help with edema?

How Does Drinking Water Help to Treat Swollen Legs and Feet? North Atlanta Vascular Clinic and Vein Center Swelling caused by fluid retention is medically known as edema. Though it can affect any part of the body, it is mostly seen in the feet, hands, arms, legs, and ankles. and feet can be caused by some medications and underlying medical conditions, including venous insufficiency.

Although prescription medications and creams can treat edema, it is essential to drink enough water. When your body is not hydrated enough, it holds onto the fluid it already has to make up for the lack of incoming water, thus contributing to swelling. Additionally, drinking more water help improves your kidney function.

You can also eat vegetables and fresh fruits to increase fluids in your body.

How do you drain edema fluid?

What are the treatments for lymphoedema? – If you think you have lymphoedema, speak to your doctor or nurse about your concerns. If it’s a new problem, they can offer you tests to find out what’s causing the lymphoedema. They can also refer you to a specialist team for assessment, if one is available in your area.

Compression – wearing special clothing or bandages that gently squeeze the part of your body that’s affected and encourage the fluid to drain away. Massage – a special type of massage called Manual Lymphatic Drainage encourages the fluid to drain away. This massage can be done by yourself, a carer or family member, or by a healthcare professional. Skin care – keep your skin clean and moisturised. Clean any cuts or scratches with an antiseptic and cover them with a plaster – this can help to reduce the risk of infection. If you have lymphoedema in your arm or leg, it’s important to have blood tests or blood pressure tests done on the affected arm or leg. Exercise – moving your body, even a little bit, helps the lymphatic fluid to drain away.

Diuretics (water tablets) are not recommended in the treatment of lymphoedema. There are also specialist treatments available in some areas. Your doctor, nurse, or lymphoedema specialist will help you find the techniques that work best for you.

Does inflammation hold water weight?

Inflammation is what happens in your body when it’s fighting something harmful, such as infections, injuries, and toxins. When something is damaging your cells, your body releases chemicals that trigger a response from your immune system. However, it can be damaging and cause increased water weight.

Can lack of water cause inflammation?

How Water Impacts Your Health – When there are proper levels of fluid in the body, then the natural systems can work to deliver nutrients to the cells. Additionally, hydration is important for protecting vital organs and tissues throughout the body. Good hydration affects blood volume and circulation, which can help to reduce recovery times.

How much water reduces inflammation?

A Word From Verywell – There is limited research assessing water’s direct impact on arthritis, but your hydration status can affect your joint health in a number of different ways. Staying adequately hydrated and reducing inflammation could help with preventing and managing arthritis and gout flares.

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By Ashley Braun, MPH, RD Ashley Braun, MPH, RD, is a registered dietitian and public health professional with over 5 years of experience educating people on health-related topics using evidence-based information. Her experience includes educating on a wide range of conditions, including diabetes, heart disease, HIV, neurological conditions, and more. Thanks for your feedback!

What does inflammation actually look like?

What does inflammation do to the body? – Inflammation comes in two forms: acute and chronic. Acute inflammation is the short-term form of inflammation that occurs when you get an injury or contract an infection. It often shows up as redness, swelling, warmth, and pain in the affected area.

  1. Chronic inflammation refers to long-term inflammation.
  2. Over time, chronic inflammation can cause the immune system to attack healthy cells and tissue, resulting in autoimmune issues.
  3. Heart disease, arthritis, bowel diseases, diabetes, and even certain forms of cancer are linked to chronic inflammation.

So what does chronic inflammation look like in the body?