A Preliminary Report of Brain Edema in Patients with Uremia at First Hemodialysis: Evaluation by Diffusion-Weighted MR Imaging

A Preliminary Report of Brain Edema in Patients with Uremia at First Hemodialysis: Evaluation by Diffusion-Weighted MR Imaging

C.L. Chena, P.H. Laib, K.J. Choua,c, P.T. Leea,c,d, H.M. Chunga,c and H.C. Fanga,C
Division of Nephrology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwanb Department of Radiology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwanc Department of Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwand Institute of Clinical Medicine, National Cheng Kung University School of Medicine, Tainan, Taiwan

Please address correspondence to Hua-Chang Fang, MD, 386 Ta-Chung 1st Rd, Kaohsiung 813, Taiwan, ROC; e-mail: hcfang@isca.vghks.gov.tw

BACKGROUND AND PURPOSE: The dynamics of brain-water content associated with hemodialysis in patients with severe azotemia remains obscure. To investigate whether either interstitial or cytotoxic edema is responsible for dialysis disequilibrium syndrome (DDS), we used diffusion-weighted MR imaging (DWI) to measure the apparent diffusion coefficient (ADC), which is sensitive for detecting tissue water dynamics.

METHODS: Eight consecutive patients with end stage renal disease (ESRD) and blood urea nitrogen level of more than 100 mg/dL (160.9 ± 53.1 mg/dL) were recruited. Conventional MR images, DWI, and clinical manifestations were obtained before and after the 1st hemodialysis. The ADC values were determined for regions of normal-appearing gray and white matter and for regions of hyperintensity of white matter on T2-weighted MR imaging.

RESULTS: Foci of bright areas of white matter were found in all patients on T2-weighted images. The ADC values of the patients with ESRD, in white matter and gray matter before and after hemodialysis, were greater than those of the healthy controls (P < .005). Regarding the impact of hemodialysis, the ADC of frontal lobe white matter increased significantly after hemodialysis (1.09 ± 0.11 versus 1.03 ± 0.11, P = .036). We did not find the specific area of brain edema reported in posterior leukoencephalopathy and the osmotic demyelination syndrome.

CONCLUSIONS: These results suggest that severe azotemia in end stage renal disease leads to interstitial brain edema reflected as increased ADC, and the further increased ADC reflects that edema associated with 1st hemodialysis is interstitial rather than cytotoxic in nature.

American Journal of Neuroradiology 28:68-71, January 2007

Leg Edema

Leg Edema

Related Terms:

Edema, Oedema, Fluid Retention, Water Retention, Swollen Leg, Lymphedema, Lymphoedema
Leg Swelling

Leg swelling is not uncommon and has been experienced by many many people. Usually, this swelling is temporary and goes away after the underlying condition is healed.

Temporary Leg Swelling

This temporary leg swelling may be caused by an infection, burn or sunburn, insect bites, an injury to the leg such as a sprain, surgery, or even medications such a hormone drugs, steroids, blood pressure drugs. This may also be an part of the inflammatory response your body goes through it trying to protect and heal the leg from the cause of the trauma.

Long Term Leg Swelling.

Long term leg swelling is referred to as edema. This is usually related to specific medical conditions. These conditions may include diabetes, congestive heart failure, blood clot, varicose veins, kidney failure, liver failure or a number of cardio-vascular problems.

Treatment for this long term swelling is in conjunction with the treatment for the condition that caused it. Usually diuretics are also used to relieve the swelling or water-retention.

Permanent Leg Swelling

****In the situation of any permanent leg swelling whether the cause is known or unknown, the diagnoses of lymphedema must be considered****

There are several groups of people who experience leg swelling from known causes, but it doesn't go away or unknown causes where the swelling can actually get worse as time goes by.

Group One

This group includes those who have had the injuries, infections, insect bites, trauma to the leg, surgeries or reaction to a medication. When this swelling does not go away, and becomes permanent it is called secondary lymphedema.

Group Two

Another extremely large group that experiences permanent leg swelling are cancer patients, people who are morbidly obese, or those with the condition called lipedema. What causes the swelling to remain permanent is that the lymph system has been so damaged that it can no longer operate normally in removing the body's waste fluid.

In cancer patients this is the result of either removal of the lymph nodes for cancer biopsy, radiation damage to the lymph system, or damage from tumor/cancer surgeries.

This is also referred to as secondary lymphedema.

Group Three

Group three consists of people who have leg swelling from seemingly unknown reasons. There may be no injury, no cancer, no trauma, but for some reason the leg simply is swollen all the time.

The swelling may start at birth, it may begin at puberty, or may begin in the 3rd, 4th or even 5th decade of life or sometimes later.

This type of leg swelling is called primary lymphedema. It can be caused by a genetic defect, malformation or damage to the lymph system while in the womb or at birth or be part of another birth condition that also effects the lymph system.

This is an extremely serious medical condition that must be diagnosed early, and treated quickly so as to avoid painful, debilitating and even life threatening complications. Treatment should NOT include the use of diuretics.

What is Lymphedema?

Lymphedema is defined simply as an accumulation of excessive protein rich fluid in the tissues of the leg. The accumulation of fluid causes the permanent swelling caused by a defective lymph system.

A conservative estimate is that there may be 1-2 million people in the United States with some form of primary lymphedema and two to three million with secondary lymphedema.

How is Lymphedema Treated?

The preferred treatment today is decongestive therapy. The forms of therapy are complete decongestive therapy (CDT) or manual decongestive therapy (MDT), there are variances, but most involve these two type of treatment.

It is a form of massage therapy where the leg is very gently massaged to actually move the fluid out of the leg and into an area where the lymph system still functions normally.

With these massage treatments, swelling is reduced and then the patient is fitted with a pre-measured custom pressure garment to keep the swelling down and/or is taught to use compression wraps to maintain the leg size.

What are the symptoms of Lymphedema?

If you are an at risk person for leg lymphedema there are early warning signs you should be aware of. If you experience any or several of these symptoms, you should immediately make your physician aware of them.

1.) Unexplained aching, hurting or pain in the leg.
2.) Experiencing "fleeting lymphedema." This is where the limb may swell, even slightly, then return to normal. This may be a precursor to full blown leg lymphedema.
3.) Localized swelling of any area. Sometimes lymphedema may start as swelling in one area, for example the foot, or between the ankle and knee. This is an indication of early lymphatic malfunction.
4.) Any arm inflammation, redness or infection.
5.) You may experience a feeling of tightness, heaviness or weakness of the leg.

What are some of the complications of lymphedema?

1. Infections such as cellulitis, lymphangitis, erysipelas. This is due not only to the large accumulation of fluid, but it is well documented that lymphodemous limbs are localized immuno-deficient.
2. Draining wounds that leak lymphorrea which is very caustic to surrounding skin tissue and acts as a port of entry for infections.
3. Increased pain as a result of the compression of nerves usually caused by the development of fibrosis and increased build up of fluids.
4. Loss of Function due to the swelling and limb changes.
5. Depression - Psychological coping as a result of the disfigurement and debilitating effect of lymphedema.
6. Deep venous thrombosis again as a result of the pressure of the swelling and fibrosis against the vascular system. Also, can happen as a result of cellulitis, lymphangitis and infections.
7. Sepsis, Gangrene are possibilities as a result of the infections.
8. Possible amputation of the limb.
9. Pleural effusions may result if the lymphatics in the abdomen or chest are to overwhelmed to clear the lung cavity of fluids.
10. Skin complications such as splitting, plaques, susceptibility to fungus and bacterial infections.
11. Chronic localized inflammations.
12. Various cancers such as lymphoma, kaposi's sarcoma and lymphangiosarcoma (Stewart Treves Syndrome)

Can lymphedema be cured?

No, at the present time there is no cure for lymphedema. But it can be treated and managed and most of the complications can be avoided. Life with lymphedema can still be active and full, with proper treatment, patient education, and patient life style adaptation.

For extensive information on lymphedema, please visit our home page:

Lymphedema People

(c) Copyright 2005 by Pat O'Connor and Lymphedema People. Use of this information for educational purpose is encouraged and permitted. It must be available free and without charge and not used for financial renumeration or gain. Please include an acknowledgement to the author and a link to Lymphedema People.

Bacillus anthracis Edema and Lethal Toxin Have Different Hemodynamic Effects but Function Together to Worsen Shock and Outcome in a Rat Model.

Bacillus anthracis Edema and Lethal Toxin Have Different Hemodynamic Effects but Function Together to Worsen Shock and Outcome in a Rat Model.
J Infect Dis. 2007 Feb 15;195(4):572-80. Epub 2007 Jan 3.

Cui X,
Li Y,
Li X,
Laird MW,
Subramanian M,
Moayeri M,
Leppla SH,
Fitz Y,
Su J,
Sherer K,
Eichacker PQ.
Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD, 20892, USA. peichacker@mail.cc.nih.gov.

Introduction. To better define the contribution of edema toxins (ETx) and lethal toxins (LeTx) to shock with Bacillus anthracis, recombinant preparations of each were investigated alone or together in rats.

Methods and results. Lethal dose ranges (0%-100% lethality) of ETx (200-800 mu g/kg as a 24-h infusion) were higher than those of LeTx (12.5-200 mu g/kg) (P<.0001). However, compared with LeTx, similarly lethal ETx doses produced earlier and greater reductions in mean blood pressure (MBP) and increased, rather than decreased, heart rate (HR) (P<.05 for all). Combining either similar weight or lethal doses of ETx and LeTx increased the hazard ratio for death (log +/- standard error) similar to the sum calculated with the toxin's effects alone (2.6+/-1.1 observed vs. 2.9+/-1.0 calculated for similar weight and 3.1+/-1.0 vs. 3.9+/-1.5 for similar lethal doses; P=.5 for both). Early
and late during infusion, ETx and LeTx together also altered MBP and HR in patterns consistent with the sum of their individual effects.

Conclusions. ETx was ~10 times less lethal than LeTx but produced greater hypotension and added to the latter's harmful effects. These findings suggest that it may be appropriate for antitoxin therapies for B. anthracis to target both ETx and LeTx.

University of Chicago Press

* * * * * * *

Lethal and Edema Toxins in the Pathogenesis of Bacillus anthracis Septic Shock: Implications for Therapy.

Am J Respir Crit Care Med. 2007 Feb 1;175(3):211-21.

Sherer K,
Li Y,
Cui X,
Eichacker PQ.
Critical Care Medicine Department, National Institutes of Health, Building 10, Room 2C145, Bethesda, MD 20892. peichacker@cc.nih.gov.

Recent research regarding the structure and function of Bacillus anthracis lethal (LeTx) and edema (ETx) toxins provides growing insights into the pathophysiology and treatment of shock with this lethal bacteria. These are both binary-type toxins composed of protective antigen necessary for their cellular uptake and either lethal or edema factors, the toxigenic moieties.

The primary cellular receptors for protective antigen have been identified and constructed and key steps in the extracellular processing and internalization of the toxins clarified. Consistent with the lethal factor's primary action as an intracellular endopeptidase targeting mitogen-activated protein kinase kinases, growing evidence indicates that shock with this toxin does not result from an excessive inflammatory response.

In fact, the potent immunosuppressive effects of LeTx may actually contribute to the establishment and persistence of infection. Instead, shock with LeTx may be related to the direct injurious effects of lethal factor on endothelial cell function. Despite the importance of LeTx, very recent studies show that edema factor, a potent adenyl cyclase, has the ability to make a substantial contribution to shock caused by B. anthracis and works additively with LeTx.

Furthermore, ETx may contribute to the immunosuppressive effects of LeTx. Therapies under development that target several different steps in the cellular uptake and function of these two toxins have been effective in in vitro and in vivo systems. Understanding how best to apply these agents clinically and how they interact with conventional treatments should be goals for future research.

Key Words: anthrax • toxin • shock • treatment

Full Text

Levels of fibrinogen compared to crp in plasma as new marker in diagnosis of pulmonary edema of non septic origin

Levels of fibrinogen compared to crp in plasma as new marker in diagnosis of pulmonary edema of non septic origin

Harefuah. 2006 Dec;145(12):870-4, 943-4

Internal Medicine F, Western Galilee Hospital-Nahariya. Raymond.Farah@naharia.health.gov.il

INTRODUCTION:

Community-acquired pneumonia, that requires hospitalization, is a severe illness with high mortality rates, especially in cases of delay of appropriate treatment. At times, the correct diagnosis of the disease is difficult due to equivocal clinical picture or chest film, accompanying diseases that could mask or simulate the pneumonia. The aims of our study were: 1. follow-up levels of fibrinogen throughout hospitalization in the group of patients admitted to the hospital due to pneumonia and pulmonary edema of non-infectious origin; 2. an estimation opportunity using them as possible new markers for diagnosis of pneumonia and for following response to treatment.

METHODS:

Three groups of patients were studied: a group of 15 patients admitted due to pneumonia, a group of 15 patients admitted due to pulmonary edema, and a control group 15 healthy subjects. The blood samples for white blood cells count, erythrocyte sedimentation rates, levels of fibrinogen, C-reactive protein, albumin, were taken for each patient on admission, 48 and 72 hours following admission and on discharge day. The received dates were compared using Student t-test.

RESULTS:

The levels of fibrinogen were higher on admission, in the patients with pneumonia, maximally after 48 and 72 hours (P<0.001) p="0.0044),"> 0.027 for both groups in discharge day). The comparison of fibrinogen levels between groups of patients with pneumonia and pulmonary edema reveal statistically significant results at time of admission, after 48 and 72 hours but not on discharge day.

CONCLUSION:

Fibrinogens can be used as reliable markers for primary diagnosing of pneumonia or differential diagnosis from pulmonary edema, on admission and until 72 hours but not for patient follow-up throughout hospitalization period. Additional studies are needed for discovering other new markers for patient follow-up throughout hospitalization period.

PMID: 17220022 [PubMed - in process]

A Preliminary Report of Brain Edema in Patients with Uremia at First Hemodialysis

A Preliminary Report of Brain Edema in Patients with Uremia at First Hemodialysis: Evaluation by Diffusion-Weighted MR Imaging

American Journal of Neuroradiology 28:68-71, January 2007© 2007 American Society of Neuroradiology

C.L. Chena, P.H. Laib, K.J. Choua,c, P.T. Leea,c,d, H.M. Chunga,c and H.C. Fanga,C
a Division of Nephrology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwanb Department of Radiology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwanc Department of Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwand Institute of Clinical Medicine, National Cheng Kung University School of Medicine, Tainan, Taiwan

Please address correspondence to Hua-Chang Fang, MD, 386 Ta-Chung 1st Rd, Kaohsiung 813, Taiwan, ROC; e-mail: hcfang@isca.vghks.gov.tw

BACKGROUND AND PURPOSE:

The dynamics of brain-water content associated with hemodialysis in patients with severe azotemia remains obscure. To investigate whether either interstitial or cytotoxic edema is responsible for dialysis disequilibrium syndrome (DDS), we used diffusion-weighted MR imaging (DWI) to measure the apparent diffusion coefficient (ADC), which is sensitive for detecting tissue water dynamics.

METHODS:

Eight consecutive patients with end stage renal disease (ESRD) and blood urea nitrogen level of more than 100 mg/dL (160.9 ± 53.1 mg/dL) were recruited. Conventional MR images, DWI, and clinical manifestations were obtained before and after the 1st hemodialysis. The ADC values were determined for regions of normal-appearing gray and white matter and for regions of hyperintensity of white matter on T2-weighted MR imaging.

RESULTS:

Foci of bright areas of white matter were found in all patients on T2-weighted images. The ADC values of the patients with ESRD, in white matter and gray matter before and after hemodialysis, were greater than those of the healthy controls (P < .005). Regarding the impact of hemodialysis, the ADC of frontal lobe white matter increased significantly after hemodialysis (1.09 ± 0.11 versus 1.03 ± 0.11, P = .036). We did not find the specific area of brain edema reported in posterior leukoencephalopathy and the osmotic demyelination syndrome.

CONCLUSIONS:

These results suggest that severe azotemia in end stage renal disease leads to interstitial brain edema reflected as increased ADC, and the further increased ADC reflects that edema associated with 1st hemodialysis is interstitial rather than cytotoxic in nature.

Article

From marrow edema to osteonecrosis

From marrow oedema to osteonecrosis: Common paths in the development of post-transplant bone pain (Review Article).

December 2006

Elder GJ.

Centre for Transplant and Renal Research, Westmead Millennium Institute, Sydney, New South Wales, Australia.

Osteonecrosis, the calcineurin-inhibitor-induced pain syndrome and transient marrow oedema may occur after renal transplantation, are generally painful and can be diagnosed by X-ray, radionuclide scan or magnetic resonance imaging. They share features of increased intraosseous pressure, compromised vascular supply, marrow oedema and the development of a 'bone compartment syndrome'. Glucocorticoid dosage is the most commonly implicated risk factor for osteonecrosis. Mechanisms may include the differentiation of mesenchymal stem cells to adipocytes causing increased intraosseous pressure and collapse of marrow sinusoids, as well as increased osteoblast and osteocyte apoptosis. Some of these effects may be ameliorated by lipid lowering drugs. Calcineurin-inhibitors, particularly cyclosporine, may increase the risk of osteonecrosis because of vasoconstrictive effects and sirolimus may influence the development of osteonecrosis by potentiating the effects of calcineurin inhibitors or by influencing the lipid profile.

For osteonecrosis, early stages are generally managed conservatively or with core decompression sometimes accompanied by bone grafting and more recently the injection of bone morphogenic protein. The use of iloprost to improve blood flow and bisphosphonates and RANK-ligand inhibition to reduce osteoclastic resorption of remaining trabecular structures are as yet unproven strategies. Unfortunately, the rate of total hip arthroplasty remains high. For the calcineurin-inhibitor-induced pain syndrome and transient marrow oedema, calcium channel blockers, the reduction or withdrawal of calcineurin-inhibitors and core decompression have been used.

Although a lack of randomized controlled trials makes management decisions difficult, early recognition of these bone pain syndromes affords the best opportunity for avoiding prolonged pain or joint replacement surgery.

KEY WORDS: bone pain, calcineurin inhibitors, glucocorticoid, marrow oedema, osteonecrosis
transplantation

Blackwell